An anterior pituitary hormone that stimulates the ADRENAL CORTEX and its production of CORTICOSTEROIDS. ACTH is a 39-amino acid polypeptide of which the N-terminal 24-amino acid segment is identical in all species and contains the adrenocorticotrophic activity. Upon further tissue-specific processing, ACTH can yield ALPHA-MSH and corticotrophin-like intermediate lobe peptide (CLIP).
A peptide of about 41 amino acids that stimulates the release of ADRENOCORTICOTROPIC HORMONE. CRH is synthesized by neurons in the PARAVENTRICULAR NUCLEUS of the HYPOTHALAMUS. After being released into the pituitary portal circulation, CRH stimulates the release of ACTH from the PITUITARY GLAND. CRH can also be synthesized in other tissues, such as PLACENTA; ADRENAL MEDULLA; and TESTIS.
A 90-amino acid peptide derived from post-translational processing of pro-opiomelanocortin (POMC) in the PITUITARY GLAND and the HYPOTHALAMUS. It is the C-terminal fragment of POMC with lipid-mobilizing activities, such as LIPOLYSIS and steroidogenesis. Depending on the species and the tissue sites, beta-LPH may be further processed to yield active peptides including GAMMA-LIPOTROPIN; BETA-MSH; and ENDORPHINS.
Cell surface proteins that bind corticotropin-releasing hormone with high affinity and trigger intracellular changes which influence the behavior of cells. The corticotropin releasing-hormone receptors on anterior pituitary cells mediate the stimulation of corticotropin release by hypothalamic corticotropin releasing factor. The physiological consequence of activating corticotropin-releasing hormone receptors on central neurons is not well understood.
Cell surface receptors that bind CORTICOTROPIN; (ACTH, adrenocorticotropic hormone) with high affinity and trigger intracellular changes. Pharmacology suggests there may be multiple ACTH receptors. An ACTH receptor has been cloned and belongs to a subfamily of G-protein-coupled receptors. In addition to the adrenal cortex, ACTH receptors are found in the brain and immune systems.
Chemical substances having a specific regulatory effect on the activity of a certain organ or organs. The term was originally applied to substances secreted by various ENDOCRINE GLANDS and transported in the bloodstream to the target organs. It is sometimes extended to include those substances that are not produced by the endocrine glands but that have similar effects.
A synthetic peptide that is identical to the 24-amino acid segment at the N-terminal of ADRENOCORTICOTROPIC HORMONE. ACTH (1-24), a segment similar in all species, contains the biological activity that stimulates production of CORTICOSTEROIDS in the ADRENAL CORTEX.
One of the three major groups of endogenous opioid peptides. They are large peptides derived from the PRO-OPIOMELANOCORTIN precursor. The known members of this group are alpha-, beta-, and gamma-endorphin. The term endorphin is also sometimes used to refer to all opioid peptides, but the narrower sense is used here; OPIOID PEPTIDES is used for the broader group.
The main glucocorticoid secreted by the ADRENAL CORTEX. Its synthetic counterpart is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions.
Natural hormones secreted by the THYROID GLAND, such as THYROXINE, and their synthetic analogs.
The outer layer of the adrenal gland. It is derived from MESODERM and comprised of three zones (outer ZONA GLOMERULOSA, middle ZONA FASCICULATA, and inner ZONA RETICULARIS) with each producing various steroids preferentially, such as ALDOSTERONE; HYDROCORTISONE; DEHYDROEPIANDROSTERONE; and ANDROSTENEDIONE. Adrenal cortex function is regulated by pituitary ADRENOCORTICOTROPIN.
A small, unpaired gland situated in the SELLA TURCICA. It is connected to the HYPOTHALAMUS by a short stalk which is called the INFUNDIBULUM.
A major gonadotropin secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Follicle-stimulating hormone stimulates GAMETOGENESIS and the supporting cells such as the ovarian GRANULOSA CELLS, the testicular SERTOLI CELLS, and LEYDIG CELLS. FSH consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the three pituitary glycoprotein hormones (TSH, LH, and FSH), but the beta subunit is unique and confers its biological specificity.
Neuropeptides of about 40 amino acids which are structurally similar to CORTICOTROPIN-RELEASING FACTOR. Unlike CRF acting primarily through type 1 CRF RECEPTORS, urocortins signal preferentially through type 2 CRF receptors. Urocortins have wide tissue distribution from fish to mammals, and diverse functions. In mammals, urocortins can suppress food intake, delays gastric emptying, and decreases heat-induced edema.
Peptides with the ability to stimulate pigmented cells MELANOCYTES in mammals and MELANOPHORES in lower vertebrates. By stimulating the synthesis and distribution of MELANIN in these pigmented cells, they increase coloration of skin and other tissue. MSHs, derived from pro-opiomelanocortin (POMC), are produced by MELANOTROPHS in the INTERMEDIATE LOBE OF PITUITARY; CORTICOTROPHS in the ANTERIOR LOBE OF PITUITARY, and the hypothalamic neurons in the ARCUATE NUCLEUS OF HYPOTHALAMUS.
A major gonadotropin secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Luteinizing hormone regulates steroid production by the interstitial cells of the TESTIS and the OVARY. The preovulatory LUTEINIZING HORMONE surge in females induces OVULATION, and subsequent LUTEINIZATION of the follicle. LUTEINIZING HORMONE consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the three pituitary glycoprotein hormones (TSH, LH and FSH), but the beta subunit is unique and confers its biological specificity.
An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p1437)
A pair of glands located at the cranial pole of each of the two KIDNEYS. Each adrenal gland is composed of two distinct endocrine tissues with separate embryonic origins, the ADRENAL CORTEX producing STEROIDS and the ADRENAL MEDULLA producing NEUROTRANSMITTERS.
Conditions in which the production of adrenal CORTICOSTEROIDS falls below the requirement of the body. Adrenal insufficiency can be caused by defects in the ADRENAL GLANDS, the PITUITARY GLAND, or the HYPOTHALAMUS.
The interactions between the anterior pituitary and adrenal glands, in which corticotropin (ACTH) stimulates the adrenal cortex and adrenal cortical hormones suppress the production of corticotropin by the anterior pituitary.
A polypeptide hormone (84 amino acid residues) secreted by the PARATHYROID GLANDS which performs the essential role of maintaining intracellular CALCIUM levels in the body. Parathyroid hormone increases intracellular calcium by promoting the release of CALCIUM from BONE, increases the intestinal absorption of calcium, increases the renal tubular reabsorption of calcium, and increases the renal excretion of phosphates.
A collection of NEURONS, tracts of NERVE FIBERS, endocrine tissue, and blood vessels in the HYPOTHALAMUS and the PITUITARY GLAND. This hypothalamo-hypophyseal portal circulation provides the mechanism for hypothalamic neuroendocrine (HYPOTHALAMIC HORMONES) regulation of pituitary function and the release of various PITUITARY HORMONES into the systemic circulation to maintain HOMEOSTASIS.
The anterior glandular lobe of the pituitary gland, also known as the adenohypophysis. It secretes the ADENOHYPOPHYSEAL HORMONES that regulate vital functions such as GROWTH; METABOLISM; and REPRODUCTION.
A decapeptide that stimulates the synthesis and secretion of both pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE. GnRH is produced by neurons in the septum PREOPTIC AREA of the HYPOTHALAMUS and released into the pituitary portal blood, leading to stimulation of GONADOTROPHS in the ANTERIOR PITUITARY GLAND.
A 30-kDa protein synthesized primarily in the ANTERIOR PITUITARY GLAND and the HYPOTHALAMUS. It is also found in the skin and other peripheral tissues. Depending on species and tissues, POMC is cleaved by PROHORMONE CONVERTASES yielding various active peptides including ACTH; BETA-LIPOTROPIN; ENDORPHINS; MELANOCYTE-STIMULATING HORMONES; and others (GAMMA-LPH; CORTICOTROPIN-LIKE INTERMEDIATE LOBE PEPTIDE; N-terminal peptide of POMC or NPP).
Steroid hormones produced by the GONADS. They stimulate reproductive organs, germ cell maturation, and the secondary sex characteristics in the males and the females. The major sex steroid hormones include ESTRADIOL; PROGESTERONE; and TESTOSTERONE.
Hormones secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Structurally, they include polypeptide, protein, and glycoprotein molecules.
Classic quantitative assay for detection of antigen-antibody reactions using a radioactively labeled substance (radioligand) either directly or indirectly to measure the binding of the unlabeled substance to a specific antibody or other receptor system. Non-immunogenic substances (e.g., haptens) can be measured if coupled to larger carrier proteins (e.g., bovine gamma-globulin or human serum albumin) capable of inducing antibody formation.
Radioimmunoassay of proteins using antibody coupled to an immunosorbent.
The wide middle zone of the adrenal cortex. This zone produces a series of enzymes that convert PREGNENOLONE to cortisol (HYDROCORTISONE) via 17-ALPHA-HYDROXYPROGESTERONE.
Specific high affinity binding proteins for THYROID HORMONES in target cells. They are usually found in the nucleus and regulate DNA transcription. These receptors are activated by hormones that leads to transcription, cell differentiation, and growth suppression. Thyroid hormone receptors are encoded by two genes (GENES, ERBA): erbA-alpha and erbA-beta for alpha and beta thyroid hormone receptors, respectively.
A 191-amino acid polypeptide hormone secreted by the human adenohypophysis (PITUITARY GLAND, ANTERIOR), also known as GH or somatotropin. Synthetic growth hormone, termed somatropin, has replaced the natural form in therapeutic usage such as treatment of dwarfism in children with growth hormone deficiency.
A 31-amino acid peptide that is the C-terminal fragment of BETA-LIPOTROPIN. It acts on OPIOID RECEPTORS and is an analgesic. Its first four amino acids at the N-terminal are identical to the tetrapeptide sequence of METHIONINE ENKEPHALIN and LEUCINE ENKEPHALIN.
Ventral part of the DIENCEPHALON extending from the region of the OPTIC CHIASM to the caudal border of the MAMMILLARY BODIES and forming the inferior and lateral walls of the THIRD VENTRICLE.
An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.
A mobile, very volatile, highly flammable liquid used as an inhalation anesthetic and as a solvent for waxes, fats, oils, perfumes, alkaloids, and gums. It is mildly irritating to skin and mucous membranes.
An epileptic syndrome characterized by the triad of infantile spasms, hypsarrhythmia, and arrest of psychomotor development at seizure onset. The majority present between 3-12 months of age, with spasms consisting of combinations of brief flexor or extensor movements of the head, trunk, and limbs. The condition is divided into two forms: cryptogenic (idiopathic) and symptomatic (secondary to a known disease process such as intrauterine infections; nervous system abnormalities; BRAIN DISEASES, METABOLIC, INBORN; prematurity; perinatal asphyxia; TUBEROUS SCLEROSIS; etc.). (From Menkes, Textbook of Child Neurology, 5th ed, pp744-8)
A condition caused by prolonged exposure to excess levels of cortisol (HYDROCORTISONE) or other GLUCOCORTICOIDS from endogenous or exogenous sources. It is characterized by upper body OBESITY; OSTEOPOROSIS; HYPERTENSION; DIABETES MELLITUS; HIRSUTISM; AMENORRHEA; and excess body fluid. Endogenous Cushing syndrome or spontaneous hypercortisolism is divided into two groups, those due to an excess of ADRENOCORTICOTROPIN and those that are ACTH-independent.
An anti-inflammatory 9-fluoro-glucocorticoid.
A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite HYDROCORTISONE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Surgical removal or destruction of the hypophysis, or pituitary gland. (Dorland, 28th ed)
Hormones secreted by the PITUITARY GLAND including those from the anterior lobe (adenohypophysis), the posterior lobe (neurohypophysis), and the ill-defined intermediate lobe. Structurally, they include small peptides, proteins, and glycoproteins. They are under the regulation of neural signals (NEUROTRANSMITTERS) or neuroendocrine signals (HYPOTHALAMIC HORMONES) from the hypothalamus as well as feedback from their targets such as ADRENAL CORTEX HORMONES; ANDROGENS; ESTROGENS.
Hormones synthesized from amino acids. They are distinguished from INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS in that their actions are systemic.
Raised area at the infundibular region of the HYPOTHALAMUS at the floor of the BRAIN, ventral to the THIRD VENTRICLE and adjacent to the ARCUATE NUCLEUS OF HYPOTHALAMUS. It contains the terminals of hypothalamic neurons and the capillary network of hypophyseal portal system, thus serving as a neuroendocrine link between the brain and the PITUITARY GLAND.
Symptom complex due to ACTH production by non-pituitary neoplasms.
Pathological processes of the ADRENAL GLANDS.
The unfavorable effect of environmental factors (stressors) on the physiological functions of an organism. Prolonged unresolved physiological stress can affect HOMEOSTASIS of the organism, and may lead to damaging or pathological conditions.
Chemical substances which inhibit the function of the endocrine glands, the biosynthesis of their secreted hormones, or the action of hormones upon their specific sites.
Nucleus in the anterior part of the HYPOTHALAMUS.
A condition observed in WOMEN and CHILDREN when there is excess coarse body hair of an adult male distribution pattern, such as facial and chest areas. It is the result of elevated ANDROGENS from the OVARIES, the ADRENAL GLANDS, or exogenous sources. The concept does not include HYPERTRICHOSIS, which is an androgen-independent excessive hair growth.
Examinations that evaluate and monitor hormone production in the adrenal cortex.
Neoplasms which arise from or metastasize to the PITUITARY GLAND. The majority of pituitary neoplasms are adenomas, which are divided into non-secreting and secreting forms. Hormone producing forms are further classified by the type of hormone they secrete. Pituitary adenomas may also be characterized by their staining properties (see ADENOMA, BASOPHIL; ADENOMA, ACIDOPHIL; and ADENOMA, CHROMOPHOBE). Pituitary tumors may compress adjacent structures, including the HYPOTHALAMUS, several CRANIAL NERVES, and the OPTIC CHIASM. Chiasmal compression may result in bitemporal HEMIANOPSIA.
Excision of one or both adrenal glands. (From Dorland, 28th ed)
A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.
The predominant form of mammalian antidiuretic hormone. It is a nonapeptide containing an ARGININE at residue 8 and two disulfide-linked cysteines at residues of 1 and 6. Arg-vasopressin is used to treat DIABETES INSIPIDUS or to improve vasomotor tone and BLOOD PRESSURE.
A lactogenic hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). It is a polypeptide of approximately 23 kD. Besides its major action on lactation, in some species prolactin exerts effects on reproduction, maternal behavior, fat metabolism, immunomodulation and osmoregulation. Prolactin receptors are present in the mammary gland, hypothalamus, liver, ovary, testis, and prostate.
An adenine nucleotide containing one phosphate group which is esterified to both the 3'- and 5'-positions of the sugar moiety. It is a second messenger and a key intracellular regulator, functioning as a mediator of activity for a number of hormones, including epinephrine, glucagon, and ACTH.
A glycoprotein hormone secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Thyrotropin stimulates THYROID GLAND by increasing the iodide transport, synthesis and release of thyroid hormones (THYROXINE and TRIIODOTHYRONINE). Thyrotropin consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is common in the pituitary glycoprotein hormones (TSH; LUTEINIZING HORMONE and FSH), but the beta subunit is unique and confers its biological specificity.
An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.
Compounds, either natural or synthetic, which block development of the growing insect.
A system of NEURONS that has the specialized function to produce and secrete HORMONES, and that constitutes, in whole or in part, an ENDOCRINE SYSTEM or organ.
Therapeutic use of hormones to alleviate the effects of hormone deficiency.
Cell surface proteins that bind pituitary hormones with high affinity and trigger intracellular changes influencing the behavior of cells. Since many pituitary hormones are also released by neurons as neurotransmitters, these receptors are also found in the nervous system.
Almond-shaped group of basal nuclei anterior to the INFERIOR HORN OF THE LATERAL VENTRICLE of the TEMPORAL LOBE. The amygdala is part of the limbic system.
Tests that evaluate the adrenal glands controlled by pituitary hormones.
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Injections into the cerebral ventricles.
Proteins obtained from species in the class of AMPHIBIANS.
A peptide of 44 amino acids in most species that stimulates the release and synthesis of GROWTH HORMONE. GHRF (or GRF) is synthesized by neurons in the ARCUATE NUCLEUS of the HYPOTHALAMUS. After being released into the pituitary portal circulation, GHRF stimulates GH release by the SOMATOTROPHS in the PITUITARY GLAND.
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
A synthetic steroid with anabolic properties that are more pronounced than its androgenic effects. It has little progestational activity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1188)
The 17-beta-isomer of estradiol, an aromatized C18 steroid with hydroxyl group at 3-beta- and 17-beta-position. Estradiol-17-beta is the most potent form of mammalian estrogenic steroids.
Inflammation of the eyelids.
A group of hydroxycorticosteroids bearing a hydroxy group at the 17-position. Urinary excretion of these compounds is used as an index of adrenal function. They are used systemically in the free alcohol form, but with esterification of the hydroxy groups, topical effectiveness is increased.
A group of polycyclic compounds closely related biochemically to TERPENES. They include cholesterol, numerous hormones, precursors of certain vitamins, bile acids, alcohols (STEROLS), and certain natural drugs and poisons. Steroids have a common nucleus, a fused, reduced 17-carbon atom ring system, cyclopentanoperhydrophenanthrene. Most steroids also have two methyl groups and an aliphatic side-chain attached to the nucleus. (From Hawley's Condensed Chemical Dictionary, 11th ed)
Peptide hormones produced by NEURONS of various regions in the HYPOTHALAMUS. They are released into the pituitary portal circulation to stimulate or inhibit PITUITARY GLAND functions. VASOPRESSIN and OXYTOCIN, though produced in the hypothalamus, are not included here for they are transported down the AXONS to the POSTERIOR LOBE OF PITUITARY before being released into the portal circulation.
A 13-amino acid peptide derived from proteolytic cleavage of ADRENOCORTICOTROPIC HORMONE, the N-terminal segment of ACTH. ACTH (1-13) is amidated at the C-terminal to form ACTH (1-13)NH2 which in turn is acetylated to form alpha-MSH in the secretory granules. Alpha-MSH stimulates the synthesis and distribution of MELANIN in MELANOCYTES in mammals and MELANOPHORES in lower vertebrates.
The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
The amount of a substance secreted by cells or by a specific organ or organism over a given period of time; usually applies to those substances which are formed by glandular tissues and are released by them into biological fluids, e.g., secretory rate of corticosteroids by the adrenal cortex, secretory rate of gastric acid by the gastric mucosa.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
A potent androgenic steroid and major product secreted by the LEYDIG CELLS of the TESTIS. Its production is stimulated by LUTEINIZING HORMONE from the PITUITARY GLAND. In turn, testosterone exerts feedback control of the pituitary LH and FSH secretion. Depending on the tissues, testosterone can be further converted to DIHYDROTESTOSTERONE or ESTRADIOL.
A glycoprotein that causes regression of MULLERIAN DUCTS. It is produced by SERTOLI CELLS of the TESTES. In the absence of this hormone, the Mullerian ducts develop into structures of the female reproductive tract. In males, defects of this hormone result in persistent Mullerian duct, a form of MALE PSEUDOHERMAPHRODITISM.
Hormones produced by the GONADS, including both steroid and peptide hormones. The major steroid hormones include ESTRADIOL and PROGESTERONE from the OVARY, and TESTOSTERONE from the TESTIS. The major peptide hormones include ACTIVINS and INHIBINS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
High affinity receptors for THYROID HORMONES, especially TRIIODOTHYRONINE. These receptors are usually found in the nucleus where they regulate DNA transcription. They are encoded by the THRB gene (also known as NR1A2, THRB1, or ERBA2 gene) as several isoforms produced by alternative splicing. Mutations in the THRB gene cause THYROID HORMONE RESISTANCE SYNDROME.
Feeling or emotion of dread, apprehension, and impending disaster but not disabling as with ANXIETY DISORDERS.
A subclass of anhydrides with the general structure of dihydrofurandione. They can be substituted on any carbon atom. They modify and inhibit proteins and enzymes and are used in the acylation of amino- and hydroxyl groups.
Elements of limited time intervals, contributing to particular results or situations.
The rate dynamics in chemical or physical systems.
A 14-amino acid peptide named for its ability to inhibit pituitary GROWTH HORMONE release, also called somatotropin release-inhibiting factor. It is expressed in the central and peripheral nervous systems, the gut, and other organs. SRIF can also inhibit the release of THYROID-STIMULATING HORMONE; PROLACTIN; INSULIN; and GLUCAGON besides acting as a neurotransmitter and neuromodulator. In a number of species including humans, there is an additional form of somatostatin, SRIF-28 with a 14-amino acid extension at the N-terminal.
Stress wherein emotional factors predominate.
The major progestational steroid that is secreted primarily by the CORPUS LUTEUM and the PLACENTA. Progesterone acts on the UTERUS, the MAMMARY GLANDS and the BRAIN. It is required in EMBRYO IMPLANTATION; PREGNANCY maintenance, and the development of mammary tissue for MILK production. Progesterone, converted from PREGNENOLONE, also serves as an intermediate in the biosynthesis of GONADAL STEROID HORMONES and adrenal CORTICOSTEROIDS.
HORMONES secreted by the gastrointestinal mucosa that affect the timing or the quality of secretion of digestive enzymes, and regulate the motor activity of the digestive system organs.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
Neural nuclei situated in the septal region. They have afferent and cholinergic efferent connections with a variety of FOREBRAIN and BRAIN STEM areas including the HIPPOCAMPAL FORMATION, the LATERAL HYPOTHALAMUS, the tegmentum, and the AMYGDALA. Included are the dorsal, lateral, medial, and triangular septal nuclei, septofimbrial nucleus, nucleus of diagonal band, nucleus of anterior commissure, and the nucleus of stria terminalis.
A group of CORTICOSTEROIDS that affect carbohydrate metabolism (GLUCONEOGENESIS, liver glycogen deposition, elevation of BLOOD SUGAR), inhibit ADRENOCORTICOTROPIC HORMONE secretion, and possess pronounced anti-inflammatory activity. They also play a role in fat and protein metabolism, maintenance of arterial blood pressure, alteration of the connective tissue response to injury, reduction in the number of circulating lymphocytes, and functioning of the central nervous system.
A multiribosomal structure representing a linear array of RIBOSOMES held together by messenger RNA; (RNA, MESSENGER); They represent the active complexes in cellular protein synthesis and are able to incorporate amino acids into polypeptides both in vivo and in vitro. (From Rieger et al., Glossary of Genetics: Classical and Molecular, 5th ed)
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A hormone secreted by the ADRENAL CORTEX that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium.
An enzyme of the lyase class that catalyzes the formation of CYCLIC AMP and pyrophosphate from ATP. EC
A gastrointestinal peptide hormone of about 43-amino acids. It is found to be a potent stimulator of INSULIN secretion and a relatively poor inhibitor of GASTRIC ACID secretion.
Use of a device for the purpose of controlling movement of all or part of the body. Splinting and casting are FRACTURE FIXATION.
Antidiuretic hormones released by the NEUROHYPOPHYSIS of all vertebrates (structure varies with species) to regulate water balance and OSMOLARITY. In general, vasopressin is a nonapeptide consisting of a six-amino-acid ring with a cysteine 1 to cysteine 6 disulfide bridge or an octapeptide containing a CYSTINE. All mammals have arginine vasopressin except the pig with a lysine at position 8. Vasopressin, a vasoconstrictor, acts on the KIDNEY COLLECTING DUCTS to increase water reabsorption, increase blood volume and blood pressure.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
Any of the ruminant mammals with curved horns in the genus Ovis, family Bovidae. They possess lachrymal grooves and interdigital glands, which are absent in GOATS.
Established cell cultures that have the potential to propagate indefinitely.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
High affinity receptors for THYROID HORMONES, especially TRIIODOTHYRONINE. These receptors are usually found in the nucleus where they regulate DNA transcription. They are encoded by the THRA gene (also known as NR1A1, THRA1, ERBA or ERBA1 gene) as several isoforms produced by alternative splicing.
The increase in a measurable parameter of a PHYSIOLOGICAL PROCESS, including cellular, microbial, and plant; immunological, cardiovascular, respiratory, reproductive, urinary, digestive, neural, musculoskeletal, ocular, and skin physiological processes; or METABOLIC PROCESS, including enzymatic and other pharmacological processes, by a drug or other chemical.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
The alpha chain of pituitary glycoprotein hormones (THYROTROPIN; FOLLICLE STIMULATING HORMONE; LUTEINIZING HORMONE) and the placental CHORIONIC GONADOTROPIN. Within a species, the alpha subunits of these four hormones are identical; the distinct functional characteristics of these glycoprotein hormones are determined by the unique beta subunits. Both subunits, the non-covalently bound heterodimers, are required for full biologic activity.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Hormones secreted by insects. They influence their growth and development. Also synthetic substances that act like insect hormones.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Peptides, natural or synthetic, that stimulate the release of PITUITARY HORMONES. They were first isolated from the extracts of the HYPOTHALAMUS; MEDIAN EMINENCE; PITUITARY STALK; and NEUROHYPOPHYSIS. In addition, some hypophysiotropic hormones control pituitary cell differentiation, cell proliferation, and hormone synthesis. Some can act on more than one pituitary hormone.
Hormones produced by invertebrates, usually insects, mollusks, annelids, and helminths.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
Hormones released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). They include a number of peptides which are formed in the NEURONS in the HYPOTHALAMUS, bound to NEUROPHYSINS, and stored in the nerve terminals in the posterior pituitary. Upon stimulation, these peptides are released into the hypophysial portal vessel blood.
A 36-amino acid peptide present in many organs and in many sympathetic noradrenergic neurons. It has vasoconstrictor and natriuretic activity and regulates local blood flow, glandular secretion, and smooth muscle activity. The peptide also stimulates feeding and drinking behavior and influences secretion of pituitary hormones.
A long-acting derivative of cyclic AMP. It is an activator of cyclic AMP-dependent protein kinase, but resistant to degradation by cyclic AMP phosphodiesterase.
Cell surface proteins that bind GROWTH HORMONE with high affinity and trigger intracellular changes influencing the behavior of cells. Activation of growth hormone receptors regulates amino acid transport through cell membranes, RNA translation to protein, DNA transcription, and protein and amino acid catabolism in many cell types. Many of these effects are mediated indirectly through stimulation of the release of somatomedins.
The active sympathomimetic hormone from the ADRENAL MEDULLA. It stimulates both the alpha- and beta- adrenergic systems, causes systemic VASOCONSTRICTION and gastrointestinal relaxation, stimulates the HEART, and dilates BRONCHI and cerebral vessels. It is used in ASTHMA and CARDIAC FAILURE and to delay absorption of local ANESTHETICS.
The regular recurrence, in cycles of about 24 hours, of biological processes or activities, such as sensitivity to drugs and stimuli, hormone secretion, sleeping, and feeding.
Compounds that interact with ESTROGEN RECEPTORS in target tissues to bring about the effects similar to those of ESTRADIOL. Estrogens stimulate the female reproductive organs, and the development of secondary female SEX CHARACTERISTICS. Estrogenic chemicals include natural, synthetic, steroidal, or non-steroidal compounds.
The biosynthesis of PEPTIDES and PROTEINS on RIBOSOMES, directed by MESSENGER RNA, via TRANSFER RNA that is charged with standard proteinogenic AMINO ACIDS.
The functions of the skin in the human and animal body. It includes the pigmentation of the skin.
Hormones produced in the testis.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
The observable response an animal makes to any situation.
The beta subunit of follicle stimulating hormone. It is a 15-kDa glycopolypeptide. Full biological activity of FSH requires the non-covalently bound heterodimers of an alpha and a beta subunit. Mutation of the FSHB gene causes delayed puberty, or infertility.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA.
A parathyroid hormone receptor subtype that recognizes both PARATHYROID HORMONE and PARATHYROID HORMONE-RELATED PROTEIN. It is a G-protein-coupled receptor that is expressed at high levels in BONE and in KIDNEY.
Insoluble polymers of TYROSINE derivatives found in and causing darkness in skin (SKIN PIGMENTATION), hair, and feathers providing protection against SUNBURN induced by SUNLIGHT. CAROTENES contribute yellow and red coloration.
A mitochondrial cytochrome P450 enzyme that catalyzes the side-chain cleavage of C27 cholesterol to C21 pregnenolone in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP11A1 gene, catalyzes the breakage between C20 and C22 which is the initial and rate-limiting step in the biosynthesis of various gonadal and adrenal steroid hormones.
Hormones produced by the placenta include CHORIONIC GONADOTROPIN, and PLACENTAL LACTOGEN as well as steroids (ESTROGENS; PROGESTERONE), and neuropeptide hormones similar to those found in the hypothalamus (HYPOTHALAMIC HORMONES).
Peptide hormones secreted into the blood by cells in the ISLETS OF LANGERHANS of the pancreas. The alpha cells secrete glucagon; the beta cells secrete insulin; the delta cells secrete somatostatin; and the PP cells secrete pancreatic polypeptide.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
Cell surface proteins that bind signalling molecules external to the cell with high affinity and convert this extracellular event into one or more intracellular signals that alter the behavior of the target cell (From Alberts, Molecular Biology of the Cell, 2nd ed, pp693-5). Cell surface receptors, unlike enzymes, do not chemically alter their ligands.
The injection of very small amounts of fluid, often with the aid of a microscope and microsyringes.
Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.
The sum of the weight of all the atoms in a molecule.
The surgical removal of one or both ovaries.
Cell surface receptors that bind thyrotropin releasing hormone (TRH) with high affinity and trigger intracellular changes which influence the behavior of cells. Activated TRH receptors in the anterior pituitary stimulate the release of thyrotropin (thyroid stimulating hormone, TSH); TRH receptors on neurons mediate neurotransmission by TRH.
Collections of small neurons centrally scattered among many fibers from the level of the TROCHLEAR NUCLEUS in the midbrain to the hypoglossal area in the MEDULLA OBLONGATA.
The reproductive organ (GONADS) in female animals. In vertebrates, the ovary contains two functional parts: the OVARIAN FOLLICLE for the production of female germ cells (OOGENESIS); and the endocrine cells (GRANULOSA CELLS; THECA CELLS; and LUTEAL CELLS) for the production of ESTROGENS and PROGESTERONE.
Cell surface proteins that bind PARATHYROID HORMONE with high affinity and trigger intracellular changes which influence the behavior of cells. Parathyroid hormone receptors on BONE; KIDNEY; and gastrointestinal cells mediate the hormone's role in calcium and phosphate homeostasis.
One of the three major families of endogenous opioid peptides. The enkephalins are pentapeptides that are widespread in the central and peripheral nervous systems and in the adrenal medulla.
The biosynthesis of RNA carried out on a template of DNA. The biosynthesis of DNA from an RNA template is called REVERSE TRANSCRIPTION.
Induction of a stress reaction in experimental subjects by means of an electrical shock; applies to either convulsive or non-convulsive states.
A technique that localizes specific nucleic acid sequences within intact chromosomes, eukaryotic cells, or bacterial cells through the use of specific nucleic acid-labeled probes.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
A disorder with chronic or recurrent colonic symptoms without a clearcut etiology. This condition is characterized by chronic or recurrent ABDOMINAL PAIN, bloating, MUCUS in FECES, and an erratic disturbance of DEFECATION.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
A well-characterized basic peptide believed to be secreted by the liver and to circulate in the blood. It has growth-regulating, insulin-like, and mitogenic activities. This growth factor has a major, but not absolute, dependence on GROWTH HORMONE. It is believed to be mainly active in adults in contrast to INSULIN-LIKE GROWTH FACTOR II, which is a major fetal growth factor.
A highly vascularized endocrine gland consisting of two lobes joined by a thin band of tissue with one lobe on each side of the TRACHEA. It secretes THYROID HORMONES from the follicular cells and CALCITONIN from the parafollicular cells thereby regulating METABOLISM and CALCIUM level in blood, respectively.
Receptors with a 6-kDa protein on the surfaces of cells that secrete LUTEINIZING HORMONE or FOLLICLE STIMULATING HORMONE, usually in the adenohypophysis. LUTEINIZING HORMONE-RELEASING HORMONE binds to these receptors, is endocytosed with the receptor and, in the cell, triggers the release of LUTEINIZING HORMONE or FOLLICLE STIMULATING HORMONE by the cell. These receptors are also found in rat gonads. INHIBINS prevent the binding of GnRH to its receptors.
Liquid chromatographic techniques which feature high inlet pressures, high sensitivity, and high speed.
A gonadotropic glycoprotein hormone produced primarily by the PLACENTA. Similar to the pituitary LUTEINIZING HORMONE in structure and function, chorionic gonadotropin is involved in maintaining the CORPUS LUTEUM during pregnancy. CG consists of two noncovalently linked subunits, alpha and beta. Within a species, the alpha subunit is virtually identical to the alpha subunits of the three pituitary glycoprotein hormones (TSH, LH, and FSH), but the beta subunit is unique and confers its biological specificity (CHORIONIC GONADOTROPIN, BETA SUBUNIT, HUMAN).
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
An inherited autosomal recessive trait, characterized by peripheral resistance to THYROID HORMONES and the resulting elevation in serum levels of THYROXINE and TRIIODOTHYRONINE. This syndrome is caused by mutations of gene THRB encoding the THYROID HORMONE RECEPTORS BETA in target cells. HYPOTHYROIDISM in these patients is partly overcome by the increased thyroid hormone levels.
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
Refers to animals in the period of time just after birth.
Cellular DNA-binding proteins encoded by the c-fos genes (GENES, FOS). They are involved in growth-related transcriptional control. c-fos combines with c-jun (PROTO-ONCOGENE PROTEINS C-JUN) to form a c-fos/c-jun heterodimer (TRANSCRIPTION FACTOR AP-1) that binds to the TRE (TPA-responsive element) in promoters of certain genes.
Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant COLEUS FORSKOHLII. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.
The relationship between the chemical structure of a compound and its biological or pharmacological activity. Compounds are often classed together because they have structural characteristics in common including shape, size, stereochemical arrangement, and distribution of functional groups.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)
The physiological period following the MENOPAUSE, the permanent cessation of the menstrual life.
A polypeptide that is secreted by the adenohypophysis (PITUITARY GLAND, ANTERIOR). Growth hormone, also known as somatotropin, stimulates mitosis, cell differentiation and cell growth. Species-specific growth hormones have been synthesized.
Cell surface proteins that bind FOLLICLE STIMULATING HORMONE with high affinity and trigger intracellular changes influencing the behavior of cells.
Cell surface receptors that bind the hypothalamic hormones regulating pituitary cell differentiation, proliferation, and hormone synthesis and release, including the pituitary-releasing and release-inhibiting hormones. The pituitary hormone-regulating hormones are also released by cells other than hypothalamic neurons, and their receptors also occur on non-pituitary cells, especially brain neurons, where their role is less well understood. Receptors for dopamine, which is a prolactin release-inhibiting hormone as well as a common neurotransmitter, are not included here.
The beta subunit of luteinizing hormone. It is a 15-kDa glycopolypeptide with structure similar to the beta subunit of the placental chorionic gonadatropin (CHORIONIC GONADOTROPIN, BETA SUBUNIT, HUMAN) except for the additional 31 amino acids at the C-terminal of CG-beta. Full biological activity of LH requires the non-covalently bound heterodimers of an alpha and a beta subunit. Mutation of the LHB gene causes HYPOGONADISM and infertility.
Compounds that interact with PROGESTERONE RECEPTORS in target tissues to bring about the effects similar to those of PROGESTERONE. Primary actions of progestins, including natural and synthetic steroids, are on the UTERUS and the MAMMARY GLAND in preparation for and in maintenance of PREGNANCY.
Organic compounds that generally contain an amino (-NH2) and a carboxyl (-COOH) group. Twenty alpha-amino acids are the subunits which are polymerized to form proteins.
A hemeprotein that catalyzes the oxidation of the iodide radical to iodine with the subsequent iodination of many organic compounds, particularly proteins. EC
Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include, but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.
Test for tissue antigen using either a direct method, by conjugation of antibody with fluorescent dye (FLUORESCENT ANTIBODY TECHNIQUE, DIRECT) or an indirect method, by formation of antigen-antibody complex which is then labeled with fluorescein-conjugated anti-immunoglobulin antibody (FLUORESCENT ANTIBODY TECHNIQUE, INDIRECT). The tissue is then examined by fluorescence microscopy.
The physical activity of a human or an animal as a behavioral phenomenon.
A 28-amino acid, acylated, orexigenic peptide that is a ligand for GROWTH HORMONE SECRETAGOGUE RECEPTORS. Ghrelin is widely expressed but primarily in the stomach in the adults. Ghrelin acts centrally to stimulate growth hormone secretion and food intake, and peripherally to regulate energy homeostasis. Its large precursor protein, known as appetite-regulating hormone or motilin-related peptide, contains ghrelin and obestatin.
The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.
Serum that contains antibodies. It is obtained from an animal that has been immunized either by ANTIGEN injection or infection with microorganisms containing the antigen.
Humoral factors secreted by the thymus gland. They participate in the development of the lymphoid system and the maturation of the cellular immune response.
A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511)
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Surgical removal or artificial destruction of gonads.
Immunoglobulin molecules having a specific amino acid sequence by virtue of which they interact only with the ANTIGEN (or a very similar shape) that induced their synthesis in cells of the lymphoid series (especially PLASMA CELLS).
The lipid- and protein-containing, selectively permeable membrane that surrounds the cytoplasm in prokaryotic and eukaryotic cells.
A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in ALCOHOLIC BEVERAGES.
A primary, chronic disease with genetic, psychosocial, and environmental factors influencing its development and manifestations. The disease is often progressive and fatal. It is characterized by impaired control over drinking, preoccupation with the drug alcohol, use of alcohol despite adverse consequences, and distortions in thinking, most notably denial. Each of these symptoms may be continuous or periodic. (Morse & Flavin for the Joint Commission of the National Council on Alcoholism and Drug Dependence and the American Society of Addiction Medicine to Study the Definition and Criteria for the Diagnosis of Alcoholism: in JAMA 1992;268:1012-4)
Electrophoresis in which a polyacrylamide gel is used as the diffusion medium.

Potent mast cell degranulation and vascular permeability triggered by urocortin through activation of corticotropin-releasing hormone receptors. (1/1772)

Urocortin (Ucn) is related to corticotropin-releasing hormone (CRH), and both are released in the brain under stress where they stimulate CRH 1 and 2 receptors (CRHR). Outside the brain, they may have proinflammatory actions through activation of mast cells, which are located perivascularly close to nerve endings and degranulate in response to acute psychological stress. Here, we report that a concentration of intradermal Ucn as low as 10 nM induced dose-dependent rat skin mast cell degranulation and increased vascular permeability. This effect appeared to be equipotent to that of calcitonin gene-related peptide and neurotensin. Ucn-induced skin vasodilation was inhibited by pretreatment with the mast cell stabilizer disodium cromoglycate (cromolyn) and was absent in the mast cell-deficient W/Wv mice. The selective nonpeptide CRH receptor 1 antagonist, antalarmin and the nonselective peptide antagonist astressin both reduced vascular permeability triggered by Ucn but not that by Substance P or histamine. In contrast, the peptide antagonist alpha-helical CRH-(9-41) reduced the effect of all three. The vasodilatory effect of Ucn was largely inhibited by pretreatment with H1 receptor antagonists, suggesting that histamine is the major mediator involved in vitro. Neuropeptide depletion of sensory neurons, treatment with the ganglionic blocker hexamethonium, or in situ skin infiltration with the local anesthetic lidocaine did not affect Ucn-induced vascular permeability, indicating that its in situ effect was not mediated through the peripheral nervous system. These results indicate that Ucn is one of the most potent triggers of rat mast cell degranulation and skin vascular permeability. This effect of Ucn may explain stress-induced disorders, such as atopic dermatitis or psoriasis, and may lead to new forms of treatment.  (+info)

Studies of the role of endothelium-dependent nitric oxide release in the sustained vasodilator effects of corticotrophin releasing factor and sauvagine. (2/1772)

1. The mechanisms of the sustained vasodilator actions of corticotrophin-releasing factor (CRF) and sauvagine (SVG) were studied using rings of endothelium de-nuded rat thoracic aorta (RTA) and the isolated perfused rat superior mesenteric arterial vasculature (SMA). 2. SVG was approximately 50 fold more potent than CRF on RTA (EC40: 0.9 +/- 0.2 and 44 +/- 9 nM respectively, P < 0.05), and approximately 10 fold more active in the perfused SMA (ED40: 0.05 +/- 0.02 and 0.6 +/- 0.1 nmol respectively, P < 0.05). Single bolus injections of CRF (100 pmol) or SVG (15 pmol) in the perfused SMA caused reductions in perfusion pressure of 23 +/- 1 and 24 +/- 2% that lasted more than 20 min. 3. Removal of the endothelium in the perfused SMA with deoxycholic acid attenuated the vasodilatation and revealed two phases to the response; a short lasting direct action, and a sustained phase which was fully inhibited. 4. Inhibition of nitric oxide synthase with L-NAME (100 microM) L-NMMA (100 microM) or 2-ethyl-2-thiopseudourea (ETPU, 100 microM) had similar effects on the vasodilator responses to CRF as removal of the endothelium, suggesting a pivotal role for nitric oxide. However the selective guanylate cyclase inhibitor 1H-[l,2,4]oxadiazolo[4,3-alpha]quinoxalin-1-one (ODQ, 10 microM) did not affect the response to CRF. 5. High potassium (60 mM) completely inhibited the vasodilator response to CRF in the perfused SMA, indicating a role for K channels in this response. 6. Compared to other vasodilator agents acting via the release of NO, the actions of CRF and SVG are strikingly long-lasting, suggesting a novel mechanism of prolonged activation of nitric oxide synthase.  (+info)

Effect of central corticotropin-releasing factor on carbon tetrachloride-induced acute liver injury in rats. (3/1772)

Central neuropeptides play important roles in many instances of physiological and pathophysiological regulation mediated through the autonomic nervous system. In regard to the hepatobiliary system, several neuropeptides act in the brain to regulate bile secretion, hepatic blood flow, and hepatic proliferation. Stressors and sympathetic nerve activation are reported to exacerbate experimental liver injury. Some stressors are known to stimulate corticotropin-releasing factor (CRF) synthesis in the central nervous system and induce activation of sympathetic nerves in animal models. The effect of intracisternal CRF on carbon tetrachloride (CCl4)-induced acute liver injury was examined in rats. Intracisternal injection of CRF dose dependently enhanced elevation of the serum alanine aminotransferase (ALT) level induced by CCl4. Elevations of serum aspartate aminotransferase, alkaline phosphatase, and total bilirubin levels by CCl4 were also enhanced by intracisternal CRF injection. Intracisternal injection of CRF also aggravated CCl4-induced hepatic histological changes. Intracisternal CRF injection alone did not modify the serum ALT level. Intravenous administration of CRF did not influence CCl4-induced acute liver injury. The aggravating effect of central CRF on CCl4-induced acute liver injury was abolished by denervation of hepatic plexus with phenol and by denervation of noradrenergic fibers with 6-hydroxydopamine treatment but not by hepatic branch vagotomy or atropine treatment. These results suggest that CRF acts in the brain to exacerbate acute liver injury through the sympathetic-noradrenergic pathways.  (+info)

Corticotropin-releasing factor receptor 1 in mouse spleen: expression after immune stimulation and identification of receptor-bearing cells. (4/1772)

A specific polyclonal Ab against the N-terminal domain of corticotropin-releasing factor (CRF) receptor, type 1 (CRF-R1), was employed to an immunohistochemical analysis of the spleen from naive mice and mice exposed to an immune challenge. Cell types stained with anti-CRF-R1 Ab were identified by their nuclear shapes and colocalization with the cell type-specific markers ER-MP58, ER-MP20, Moma-1, Moma 2, anti-CD3e mAbs, and anti-Ig Ab. Only a few clusters of CRF-R1+ cells were found in spleen sections of naive mice at sites typical for granulopoietic islands. However, a 17-fold increase in the mean number of CRF-R1+ cells was noted within hours following a challenge of acute systemic inflammation induced by i.p. administration of LPS. The majority of these cells were identified as mature neutrophils. CRF-R1 was shown to mediate suppression of the IL-1beta secretion by these cells. However, at later time points a large number of granulocyte-macrophage precursors was strongly labeled with anti-CRF-R1 Ab. Western blot analysis of splenic membranes from animals treated with LPS revealed a m.w. of approximately 70,000 for CRF-R1. Subcellular staining patterns were suggestive for the predominant localization of CRF-R1 on granule membranes. CRF-R1 mRNA was detected in spleen but not in bone marrow and peripheral blood leukocytes from naive mice. Thus, it was indicated that CRF-R1 was not produced constitutively by mature or immature neutrophils. Its production was rather triggered by inflammatory stimuli.  (+info)

Evaluation of hypothalamic-pituitary-adrenal axis in amenorrhoeic women with insulin-dependent diabetes. (5/1772)

Diabetes is associated with a higher incidence of secondary hypogonadotrophic amenorrhoea. In amenorrhoeic women with insulin-dependent diabetes a derangement in hypothalamic-pituitary-ovary axis has been proposed. No data exist on hypothalamic-pituitary-adrenal function in these women. Gonadotrophin releasing hormone (GnRH), corticotrophin releasing hormone (CRH), metoclopramide and thyroid releasing hormone (TRH) tests were performed in 15 diabetic women, eight amenorrhoeic (AD) and seven eumenorrhoeic (ED). Frequent blood samples were taken during 24 h to evaluate cortisol plasma concentrations. There were no differences between the groups in body mass index, duration of diabetes, insulin dose and metabolic control. The AD women had lower plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), prolactin, oestradiol, androstenedione and 17-hydroxyprogesterone (17-OHP) than the ED women. The responses of pituitary gonadotrophins to GnRH, and of thyroid stimulating hormone (TSH) to TRH, were similar in both groups. The AD women had a lower prolactin response to TRH and metoclopramide, and lower ACTH and cortisol responses to CRH, than the ED women. Mean cortisol concentrations > 24 h were higher in the amenorrhoeic group. Significant differences in cortisol concentrations from 2400 to 1000 h were found between the two groups. Insulin-dependent diabetes may involve mild chronic hypercortisolism which may affect metabolic control. Stress-induced activation of the hypothalamic-pituitary-adrenal axis would increase hypothalamic secretion of CRH. This would lead directly and perhaps also indirectly by increasing dopaminergic tonus to inhibition of GnRH secretion and hence hypogonadotrophic amenorrhoea. Amenorrhoea associated with metabolically controlled insulin-dependent diabetes is a form of functional hypothalamic amenorrhoea that requires pharmacological and psychological management.  (+info)

Pituitary-adrenal cortical responses to low-dose physostigmine and arginine vasopressin administration in normal women and men. (6/1772)

Animal studies indicate that central cholinergic neurotransmission stimulates CRH secretion, but several human studies suggest that the hypothalamo-pituitary-adrenal cortical (HPA) axis may be activated only by doses of cholinergic agonists that produce noxious side effects and, by inference, a nonspecific stress response. Physostigmine (PHYSO), a reversible cholinesterase inhibitor, was administered to normal women and men at a dose that elevated plasma ACTH1-39, cortisol, and arginine vasopressin (AVP) concentrations but produced few or no side effects. Exogenous AVP also was administered alone and following PHYSO, to determine if it would augment the effect of PHYSO on the HPA axis. Fourteen normal women and 14 normal men matched to the women on age and race underwent four test sessions 5 to 7 days apart: PHYSO (8 micrograms/kg i.v.), AVP (0.08 U/kg i.m.), PHYSO plus AVP, and saline control. Serial blood samples taken before and after pharmacologic challenge were analyzed for ACTH1-39, cortisol, and AVP. PHYSO and AVP administration produced no side effects in about half the subjects and mild side effects in the other half, with no significant female-male differences overall. There also were no significant female-male differences in ACTH1-39 or cortisol responses to AVP. In contrast, the men had significantly greater ACTH1-39 responses to PHYSO administration than did the women. The endogenous AVP response to PHYSO also was significantly greater in the men than in the women, and the ACTH1-39 and AVP responses to PHYSO were significantly correlated in the men (both = +0.70) but not in the women. None of the hormone responses was significantly correlated with the presence or absence of side effects in either group of subjects. These results indicate a greater sensitivity of the HPA axis to low-dose PHYSO in normal men than in normal women, which likely is mediated by increased secretion of AVP. The lack of difference in side effects between the two groups of subjects and the lack of significant correlations between presence or absence of side effects and hormone responses in either group suggest that the increased hormone responses in the men were due to increased responsivity of central cholinergic systems and not to a nonspecific stress response.  (+info)

Peripheral urocortin delays gastric emptying: role of CRF receptor 2. (7/1772)

Urocortin, a new mammalian member of the corticotropin-releasing factor (CRF) family has been proposed to be the endogenous ligand for CRF receptor 2 (CRF-R2). We studied the influence of intravenous urocortin on gastric emptying and the role of CRF-R2 in peptide action and postoperative gastric ileus in conscious rats. The intravenous doses of rat CRF and rat urocortin producing 50% inhibition of gastric emptying were 2.5 and 1.1 microgram/kg, respectively. At these intravenous doses, CRF and urocortin have their actions fully reversed by the CRF-R1/CRF-R2 antagonist astressin at antagonist/agonist ratios of 5:1 and 67:1, respectively. Astressin (12 microgram/kg iv) completely prevented abdominal surgery-induced 54% inhibition of gastric emptying 3 h after surgery while having no effect on basal gastric emptying. The selective nonpeptide CRF-R1 antagonists antalarmin (20 mg/kg ip) and NBI-27914 (400 microgram/kg iv) did not influence intravenous CRF-, urocortin- or surgery-induced gastric stasis. These results as well as earlier ones showing that alpha-helical CRF9-41 (a CRF-R2 more selective antagonist) partly prevented postoperative ileus indicate that peripheral CRF-R2 may be primarily involved in intravenous urocortin-, CRF-, and abdominal surgery-induced gastric stasis.  (+info)

Mechanisms underlying the anti-inflammatory actions of central corticotropin-releasing factor. (8/1772)

Immune activation of hypothalamic corticotropin-releasing factor (CRF) provides a negative feedback mechanism to modulate peripheral inflammatory responses. We investigated whether central CRF attenuates endothelial expression of intercellular adhesion molecule 1 (ICAM-1) and leukocyte recruitment during endotoxemia in rats and determined its mechanisms of action. As measured by intravital microscopy, lipopolysaccharide (LPS) induced a dose-dependent increase in leukocyte rolling, adhesion, and emigration in mesenteric venules, which was associated with upregulation of endothelial ICAM-1 expression. Intracisternal injection of CRF abrogated both the increased expression of ICAM-1 and leukocyte recruitment. Intravenous injection of the specific CRF receptor antagonist astressin did not modify leukocyte-endothelial cell interactions induced by a high dose of LPS but enhanced leukocyte adhesion induced by a low dose. Blockade of endogenous glucocorticoids but not alpha-melanocyte-stimulating hormone (alpha-MSH) receptors reversed the inhibitory action of CRF on leukocyte-endothelial cell interactions during endotoxemia. In conclusion, cerebral CRF blunts endothelial upregulation of ICAM-1 and attenuates the recruitment of leukocytes during endotoxemia. The anti-inflammatory effects of CRF are mediated by adrenocortical activation and additional mechanisms independent of alpha-MSH.  (+info)

TY - JOUR. T1 - Histone deacetylase 1 (HDAC1) participates in the down-regulation of corticotropin releasing hormone gene (crh) expression. AU - Miller, Lydia. AU - Foradori, Chad D.. AU - Lalmansingh, Avin S.. AU - Sharma, Dharmendra. AU - Handa, Robert J.. AU - Uht, Rosalie Maire. PY - 2011/8/3. Y1 - 2011/8/3. N2 - The paraventricular nucleus of the hypothalamus (PVH) plays a central role in regulating the hypothalamic-pituitary-adrenal (HPA) axis. Medial parvocellular neurons of the PVH (mpPVH) integrate sensory and humoral inputs to maintain homeostasis. Humoral inputs include glucocorticoids secreted by the adrenals, which down-regulate HPA activation. A primary glucocorticoid target is the population of mpPVH neurons that synthesize and secrete corticotropin-releasing factors, the most potent of which is corticotropin-releasing hormone (CRH). Although CRH gene (crh) expression is known to be down-regulated by glucocorticoids, the mechanisms by which this process occurs are still poorly ...
TY - JOUR. T1 - Glucocorticoid negative feedback selectively targets vasopressin transcription in parvocellular neurosecretory neurons. AU - Kovács, Krisztina J.. AU - Földes, Anna. AU - Sawchenko, Paul E.. PY - 2000/5/15. Y1 - 2000/5/15. N2 - To identify molecular targets of corticosteroid negative feedback effects on neurosecretory neurons comprising the central limb of the hypothalamo-pituitary-adrenal (HPA) axis, we monitored ether stress effects on corticotropin-releasing factor (CRF) and arginine vasopressin (AVP) heteronuclear RNA (hnRNA) expression in rats that were intact or adrenalectomized (ADX) and replaced with corticosterone (B) at constant levels ranging from nil to peak stress concentrations. Under basal conditions, relative levels of both primary transcripts varied inversely as a function of plasma B titers. In response to stress, the kinetics of CRF hnRNA responses of intact and ADX rats replaced with low B were similar, peaking at 5 min after stress. By contrast, intact rats ...
TY - JOUR. T1 - Regulation of corticotropin-releasing factor neuronal systems and hypothalamic-pituitary-adrenal axis activity by stress and chronic antidepressant treatment. AU - Stout, Steven C.. AU - Owens, Michael J.. AU - Nemeroff, Charles B.. PY - 2002. Y1 - 2002. N2 - In a series of experiments, we tested the hypothesis that chronic antidepressant drug administration reduces the synaptic availability of corticotropin-releasing factor (CRF) through one or more effects on CRF gene expression or peptide synthesis. We also determined whether effects of acute or chronic stress on CRF gene expression or peptide concentration are influenced by antidepressant drug treatment. Four-week treatment with venlafaxine, a dual serotonin (5-HT)/norepinephrine (NE) reuptake inhibitor, and tranylcypromine, a monoamine oxidase inhibitor, resulted in an attenuation of acute stress-induced increases in CRF heteronuclear RNA (hnRNA) synthesis in the paraventricular nucleus (PVN). Trends toward the same effect ...
Read N -methyl- d -aspartate (NMDA)-mediated corticotropin-releasing factor (CRF) release in cultured rat amygdala neurons 1 1 Abbreviations used: CRF, corticotropin-releasing factor; NMDA, N -methyl- d -aspartate; AP-5, 2-amino-5-phosphonovaleric acid; LC, locus coeruleus; DIC, days in culture., Peptides on DeepDyve, the largest online rental service for scholarly research with thousands of academic publications available at your fingertips.
TY - JOUR. T1 - Cerebrospinal fluid corticotropin-releasing factor increases following haloperidol withdrawal in chronic schizophrenia. AU - Forman, Steven D.. AU - Bissette, Garth. AU - Yao, Jeffrey. AU - Nemeroff, Charles. AU - van Kammen, Daniel P.. PY - 1994/1/1. Y1 - 1994/1/1. N2 - Corticotropin-releasing factor (CRF), an endogenous neuropeptide, has been shown to coordinate endocrine, behavioral and autonomic responses to stress. However, while previous studies of cerebrospinal fluid (CSF) CRF in schizophrenia have not demonstrated significant differences compared to control groups, these studies have not examined the effects of symptom severity or antipsychotic medication. CSF CRF concentrations increased in 18 of 21 male schizophrenic (DSM-III-R) patients after maintenance haloperidol was replaced by placebo (P,0.0001); there was also a trend for relatively greater increases in relapsers. CRF concentrations were not significantly related to severity of psychosis, depression, anxiety or ...
TY - JOUR. T1 - Localization of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the human hypothalamus; age-dependent colocalization with vasopressin. AU - Raadsheer, F.C.. AU - Sluiter, A.A.. AU - Ravid, R.. AU - Tilders, F.J.H.. AU - Swaab, D.F.. PY - 1993. Y1 - 1993. M3 - Article. VL - 615. SP - 50. EP - 62. JO - Brain Research. JF - Brain Research. SN - 0006-8993. ER - ...
Author(s): Brunson, Kristen L; Grigoriadis, Dimitri E; Lorang, Marge T; Baram, Tallie Z | Abstract: In addition to regulating the neuroendocrine stress response, corticotropin-releasing hormone (CRH) has been implicated in both normal and pathological behavioral and cognitive responses to stress. CRH-expressing cells and their target neurons possessing CRH receptors (CRF1 and CRF2) are distributed throughout the limbic system, but little is known about the regulation of limbic CRH receptor function and expression, including regulation by the peptide itself. Because CRH is released from limbic neuronal terminals during stress, this regulation might play a crucial role in the mechanisms by which stress contributes to human neuropsychiatric conditions such as depression or posttraumatic stress disorder. Therefore, these studies tested the hypothesis that CRH binding to CRF1 influenced the levels and mRNA expression of this receptor in stress-associated limbic regions of immature rat. Binding capacities and
The regulatory region of the corticotropin-releasing hormone (CRH) is highly conserved across species and plays a crucial role in the response of the organism to stress. Release of CRH initiates a cascade of events leading to the release of cortisol and the regulation of inflammatory and immune events. In this report we describe polymorphisms in the 5 regulatory region of the CRH gene in humans. We studied the distribution of CRH alleles in three different African populations, in white UK Caucasoids, and in a Chinese population. In the African and UK populations we found three new polymorphisms which cosegregated, resulting in two alleles, A1 and A2. Gene frequencies for A1 and A2 were extremely divergent between the African and the UK populations. The African A1 frequency ranged from 0.27-0.3, while the UK Caucasoid frequency was 0.9. Compound alleles could be assigned by taking into account the previously described biallelic polymorphism at position 225 in the CRH promoter. The A2B1 compound allele
Autor: Linthorst, A. C. E. et al.; Genre: Zeitschriftenartikel; Im Druck veröffentlicht: 1997; Titel: Long-term intracerebroventricular infusion of corticotropin-releasing hormone alters neuroendocrine, neurochemical, autonomic, behavioral and cytokine responses to a systemic inflammatory challenge
In various animals, such as some fish, early exposure during development to environmental stressors, including high temperature, causes genetically female animals to develop male gonads. Although the process of sex reversal has been studied at a molecular level during gonad development, the role of the brain remains enigmatic. Now, Juan Fernandino and colleagues provide the first evidence that the central nervous system regulates environmental masculinisation in the medaka. They show that corticotropin-releasing hormone B (crhb) is upregulated in embryos incubated at high temperature during the period of gonadal sex determination. Using CRISPR/Cas9 to mutate the two genes encoding receptors for Crh, the authors show that mutating both crhr1 and crhr2 reduces female-to-male sex reversal at high temperatures. The process of masculinisation in these mutants can be rescued through the addition of cortisol, which acts downstream of Crh. Together, these data indicate that the ...
Background In this study the predictive value of the combined dexamethasone/CRH test (DEX/CRH test) for acute antidepressant response was investigated. Methodology/Principal Findings In 114 depressed inpatients suffering from unipolar or bipolar depression (sample 1) the DEX/CRH test was performed at admission and shortly before discharge. During their stay in the hospital patients received different antidepressant treatment regimens. At admission, the rate of nonsuppression (basal cortisol levels |75.3 nmol/l) was 24.6% and was not related to the later therapeutic response. Moreover, 45 out of 114 (39.5%) patients showed an enhancement of HPA axis function at discharge in spite of clinical improvement. In a second sample, 40 depressed patients were treated either with reboxetine or mirtazapine for 5 weeks. The DEX/CRH test was performed before, after 1 week, and after 5 weeks of pharmacotherapy. Attenuation of HPA axis activity after 1 week was associated with a more pronounced alleviation of
Rivalland, Elizabeth T.A., Iqbal, J., Clarke, I.J., Turner, Anne I. and Tilbrook, A.J. 2003, Distribution and co-localisation of corticotrophin-releasing hormone (CRH), arginine vasopressin (AVP) and enkephalin (Enk) in the paraventricular nucleus (PVN) of the ewe, in Proceedings of the Endocrine Society of Australia, Endocrine Society of Australia, Melbourne, Vic., pp. 305-305. ...
Three uncommon findings were observed in a case of Cushings disease due to macroadenoma: no suppression of plasma ACTH during an 8-mg dexamethasone test, a negative corticotropin-releasing factor tes
0.05) while circulating levels were unchanged at 3 or 4 4 h. ACTH levels rose compared to control rats (135.3 ± 13.8 vs. 101.4 ± 6.0 pg/ml; p < 0.05) 30 min after the increase in CRH while at 3 or 6 h after LPS the levels were not changed. Conclusion Intraperitoneal LPS induces a delayed rise in plasma CRH levels associated with an elevation in ACTH plasma levels 30 min later suggesting that under conditions of immune challenge CRH of peripheral origin may also contribute to pituitary activation as detected using the RAPID method of blood processing which improves CRH recovery. Blood collected as described in experimental protocols was transferred to EDTA-containing borosilicate glass tubes on ice and in parallel immediately within 7-10 min processed according to the 3 methods. The first set of Y-33075 samples was processed according to the RAPID method as detailed previously [19]. Briefly the blood was diluted 1:10 in ice-cold buffer (pH 3.6) containing 0.1 ammonium acetate 0.5 NaCl and ...
Corticotropin-releasing hormone (CRH), the principal neuropeptide regulator of pituitary ACTH secretion, is also produced at peripheral inflammatory sites, where it acts as a proinflammatory cytokine, and by the Leydig cell of the testis, where it exerts autocrine inhibition of testosterone biosynthesis. Because key ovarian functions, such as ovulation and luteolysis, represent aseptic inflammatory responses, and because the theca cell is the functional equivalent of the Leydig cell, we explored the CRH presence in the ovary, first, by specific CRH immunohistochemistry of adult cycling female Sprague-Dawley rat ovaries. We detected cytoplasmic immunoreactive CRH (IrCRH) in theca and stromal cells and in cells within the corpora lutea, at all phases of the estrous cycle. Using a specific radioimmunoassay, we measured IrCRH in extracts of rat ovaries (0.042-0.126 pmol/g wet tissue). The mobility of the ovarian IrCRH molecule was similar to that of rat/human CRH by reverse phase HPLC. To ...
The isoflavone, daidzein is a biologically active, plant-derived compound that interacts with estrogen receptors. Data from previous studies have suggested that daidzein exerts beneficial effects in many diseases; however, as an endocrine disrupter, it may also alter the functioning of the endocrine system. Data regarding the effect of daidzein on the morphofunctional and histological parameters of the hypothalamic-pituitary-adrenal (HPA) system is still lacking. Therefore, using the newCAST stereological software, we investigated the effects of chronic (21 days) daidzein treatment on corticotropin-releasing hormone (CRH) neurons within the hypothalamus and corticotropes (ACTH cells) in the pituitary, while image analysis was employed to-examine the intensity of fluorescence of CRH in the median eminence (ME) and adrenocorticotropin hormone in the pituitary in adult orchidectomized (Ovx) rats ...
Hypothalamic-pituitary-adrenal (HPA) responses remain intact or increase after chronic or repeated stress despite robust levels of circulating glucocorticoids that would be expected to restrain the responsiveness of the axis. The purpose of this study was to determine whether chronic stress altered …
In several neurological disorders including cerebral ischaemia, glutamate has been implicated as a neurotoxic agent in the mechanisms leading to neuronal cell death. The role of corticotrophin-releasing hormone (CRH), the 41-amino acid peptide, which activates the HPA axis in response to stressful stimuli, remains controversial. In this study, we report that CRH in low physiological concentrations (2 pm), prevented glutamate-induced neurotoxicity via receptor-mediated mechanisms when administered to organotypic hippocampal cultures both during and after the glutamate-induced insult. Detailed investigations on the mechanisms mediating this neuroprotective effect showed that activation of the adenylate cyclase pathway and induction of MAP kinase phosphorylation mediate the CRH action. In addition we showed that CRH can inhibit the phosphorylation of JNK/SAPK by glutamate. Most importantly, we showed that CRH can afford neuroprotection against neurotoxicity up to 12 h following the insult, ...
Subjects. The subjects were 63 male Long-Evans rats (Charles River, Raleigh, NC; 300-400 gm). Thirty-seven rats were studied for self-administration of heroin. Four of these animals developed blocked catheters, and their data are not included in the tests for reinstatement. They were, however, used for hormonal measurements at the end of the experiment. The animals were transferred from the animal housing facility to operant chambers 1 week after surgery. The animals lived in the operant chambers for 24 hr per day and were maintained on a reversed light/dark cycle (lights on 10:00 P.M. to 10:00 A.M.) throughout the experiment. Food and water were available ad libitum except during the 3 hr tests for reinstatement (see below). Twenty-six drug-naive rats were used for hormonal measurements after exposure to metyrapone and footshock. These rats were maintained on a reverse light/dark cycle in the animal facility with food and water available ad libitum. The drug-naive rats were brought to the ...
Dedic N, Kühne C, Jakovcevski M, Hartmann J, Genewsky AJ, Gomes KS, Anderzhanova E, Pöhlmann ML, Chang S, Kolarz A, Vogl AM, Dine J, Metzger MW, Schmid B, Almada RC, Ressler KJ, Wotjak CT, Grinevich V, Chen A, Schmidt MV, Wurst W, Refojo D, Deussing JM. Chronic CRH depletion from GABAergic, long-range projection neurons in the extended amygdala reduces dopamine release and increases anxiety. Nat Neurosci. 2018 06; 21(6):803-807 ...
Corticotropin-releasing hormone is a potent stimulator of synthesis and secretion of preopiomelanocortin-derived peptides. Although CRH concentrations in the human peripheral circulation are normally low, they increase throughout pregnancy and fall rapidly after parturition. Maternal plasma CRH probably originates from the placenta. Human plasma contains a CRH-binding protein which inactivates CRH and which may prevent inappropriate pituitary-adrenal stimulation in pregnancy ...
Sigma-Aldrich offers abstracts and full-text articles by [J Megan Gray, Haley A Vecchiarelli, Maria Morena, Tiffany T Y Lee, Daniel J Hermanson, Alexander B Kim, Ryan J McLaughlin, Kowther I Hassan, Claudia Kühne, Carsten T Wotjak, Jan M Deussing, Sachin Patel, Matthew N Hill].
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Dr. Koobs early research interests were directed at the neurobiology of emotion, with a focus on the theoretical constructs of reward and stress. He has made contributions to our understanding of the anatomical connections of the emotional systems and the neurochemistry of emotional function. Dr. Koob has identified afferent and efferent connections of the basal forebrain in the region of the nucleus accumbens, bed nucleus of the stria terminalis, and central nucleus of the amygdala in motor activation, reinforcement mechanisms, behavioral responses to stress, drug self-administration, and the neuroadaptation associated with drug dependence. Dr. Koobs work with the neurobiology of stress includes the characterization of behavioral functions in the central nervous system for catecholamines, opioid peptides, and corticotropin-releasing factor. Corticotropin-releasing factor, in addition to its classical hormonal functions in the hypothalamic-pituitary-adrenal axis, is also located in ...
corticotropin releasing factor-binding protein: MW 37 kDa; abolishes CRH-induced ACTH release; amino acid sequence in first source, (CRF-BP)
Labeled antagonists have advantages over agonists for the characterization of G protein-coupled receptors if, for example, the total number of binding sites is of interest, because the binding of antagonists is independent of the fraction of receptors coupled to the GTP-binding proteins (DeLean et al., 1980). For example, in thebeta adrenergic receptor system, high-affinity antagonists were used in receptor characterization (Brown et al., 1976).. All previously reported CRF antagonists were of too low an affinity to be used as radioligands for characterizing CRF-R1 receptors. With astressin (Gulyas et al., 1995), we now have an antagonist of sufficient affinity to make it suitable as a radioligand for the detection and characterization of both cloned and endogenous CRF receptors. Using autoradiographic techniques and radioreceptor assays, brain receptors have also been detected with oCRF* (De Souza et al., 1984) and 125I-labeled [Tyr0]oCRF (Grigoriadis and De Souza, 1988;Webster et al., ...
Cell Type-Specific Expression of Corticotropin-Releasing Hormone-binding Protein in Gabaergic Interneurons in the Prefrontal Cortex Ketchesin KD, Huang NS, Seasholtz AF. Front Neuroanat. 2017 Oct 10;11:90. doi: 10.3389/fnana.2017.00090. eCollection 2017
In general, when one perceives a stressful situation, the (limbic)-hypothalamic-pituitary-adrenal (HPA) axis is activated. The HPA axis is a set of neuroendocrine responses to a stressful situation. The paraventricular nucleus of the hypothalamus secretes corticotropin-releasing hormone (CRH) and vasopressin, which are both part of the neuroendocrine system, classified as neurotransmitters and hormones (...animal physiology class is all coming back...). Vasopressin is an anti-diuretic, polypeptide hormone responsible for the bodys conservation of water and plays a key role in the regulation of homeostasis. CRH is also a polypeptide hormone and is responsible for stimulating further stress hormones. CRH is carried to the anterior lobe of the pituitary gland and vasopressin to the to the posterior lobe of the pituitary. CRH stimulates the synthesis and release of adrenocorticotropic hormone (ACTH), which is then released into the bloodstream and stimulates the adrenal glands. The adrenals are two ...
The CRF1 receptor is a Gs-coupled GPCR expressed in the brain and pituitary gland that binds to several neuropeptides, including corticotropin-releasing factor (CRF) and urocortin, and the amphibian peptide sauvagine. CRF plays a predominant role in stress response mediated by the hypothalamic-pituitary-adrenal axis, and alterations in CRF and its receptors CRF1 and CRF2 appear to be linked to depression and anxiety. In comparison to the CRF2 receptor, the CRF1 receptor has received considerable attention as a potential therapeutic target for the treatment of stress-related disorders such as adrenocorticotropin hypersecretion, increased colonic motility and exaggerated fear and anxiety-related behavior.
InterPro provides functional analysis of proteins by classifying them into families and predicting domains and important sites. We combine protein signatures from a number of member databases into a single searchable resource, capitalising on their individual strengths to produce a powerful integrated database and diagnostic tool.
Figure 1: Structure of Cart peptides. Receptors involved with CART Peptides. So far, no specific CART receptor has been identified. However, there is substantial experimental evidence suggesting the existence of several CART receptor subtypes.. For example, several studies have shown that CART peptides could activate three signaling mechanisms, and that they modulate dopamine receptors-related pathways. First, CART 55-102 has been described to inhibit the voltage-gated L-type Ca2+ channels in a pertussis toxin (PTX)-sensitive manner [5]. PTX is an inhibitor of inhibitory-G-protein (Gi/Go)-dependent signaling pathways [6]. Then, CART 55-102 has been described to increase the phosphorylation of cyclic AMP-response-element-binding protein (CREB) in the nucleus of corticotropin-releasing hormone (CRH) neurons located in the hypothalamic paraventricular nucleus in rats [7]. Ultimately, it promotes the expression of the CREB and induces profound antidepressant effects. Numerous genes associated with ...
Brain, Corticotropin, Corticotropin-releasing Factor, Crf Receptor, Gastric Emptying, Norepinephrine, Neurons, Neuropeptide, Mice, Anxiety, and Hydrogen
Corticotropin-releasing hormone (CRH) is the master stress hormone. When this hormone goes awry it can impact everything, from your weight, to your health, to your behavior.
Stress can trigger drug-seeking behavior, increase self-administration rates, and enhance drug reward. A number of stress-related neuropeptides have been shown to mediate these behavioral processes. The most studied peptide in this category is corticotropin-releasing hormone (CRH), which has been sh …
ENCODES a protein that exhibits DNA binding (ortholog); DNA-binding transcription activator activity, RNA polymerase II-specific (ortholog); identical protein binding (ortholog); INVOLVED IN apoptotic process (ortholog); cell migration involved in sprouting angiogenesis (ortholog); cellular response to corticotropin-releasing hormone stimulus (ortholog); ASSOCIATED WITH Albuminuria (ortholog); blood pressure trait (ortholog); blood urea nitrogen amount (ortholog); FOUND IN cytosol (ortholog); nuclear membrane (ortholog); nucleoplasm (ortholog)
In response to stressors, individuals exhibit different coping styles, each characterized by a set of behavioral, physiological, and psychological responses.
In an attempt to clarify the role of the type 2 corticotropin-releasing hormone (CRH) receptor (CRHR-2) in the brain in activation of the hypothalamic-pituitary-adrenocortical axis, we conducted experiments using male Wistar rats. First, an injection of urocortin-2 (7.5 µg) into the lateral ventricle resulted in transient increases in CRH heteronuclear RNA (hnRNA) in parvocellular paraventricular nucleus (PVN) and in plasma adrenocorticotropic hormone (ACTH), whereas sustained increases in arginine vasopressin (AVP) hnRNA and c-fos mRNA in the parvocellular PVN were observed as compared with vehicle treatment. Pretreatment with the selective CRHR-2 antagonist antisauvagine-30 (20 µg) into the lateral ventricle 15 min prior to agonist injection attenuated the stimulatory effects of urocortin-2 on the above-mentioned hypothalamic-pituitary-adrenal axis variables. These effects were similar or rather more potent than those induced by pretreatment with 50 µg of α-helical CRH. Second, we found longer
The human CRHR2 gene contains 12 exons. Three major functional isoforms, alpha (411 amino acids), beta (438 amino acids), and gamma (397 amino acids), encoded by transcripts with alternative first exons,[7] differ only in the N-terminal sequence comprising the signal peptide and part of the extracellular domain (amino acids 18-108 of CRHR2 alpha); the unique N-terminal sequence of each isoform (34 amino acids in CRHR2 alpha; 61 amino acids in Hs CRHR2 beta; 20 amino acids in CRHR2 gamma) is followed by a sequence common to all isoforms (377 amino acids)[8] comprising most of the multi-pass transmembrane domain followed by a cytoplasmic domain of 47 amino acids. CRHR2 beta is expressed in human brain; CRHR2 alpha predominates in peripheral tissues. The N-terminal signal peptides of corticotropin-releasing hormone receptor 1 and CRHR2 beta are cleaved off in the endoplasmic reticulum to yield the mature receptors. In contrast, CRHR2 alpha contains a unique pseudo signal peptide that is not removed ...
TY - JOUR. T1 - Corticotropin-releasing hormone stimulates proopiomelanocortin transcription by cFos-dependent and -independent pathways. T2 - Characterization of an AP1 site in exon 1. AU - Boutillier, A. L.. AU - Monnier, D.. AU - Lorang, D.. AU - Lundblad, J. R.. AU - Roberts, J. L.. AU - Loeffler, J. P.. N1 - Copyright: Copyright 2016 Elsevier B.V., All rights reserved.. PY - 1995/6/1. Y1 - 1995/6/1. N2 - The POMC gene, encoding a hormonal precursor protein, is primarily expressed in the pituitary in a tissue-specific manner. The POMC gene is transcriptionally regulated by a variety of hormones and neuropeptides and the second messengers cAMP and Ca++. Using the corticotrope-derived AtT20 cell line, we have previously shown that overexpression of cFos stimulates POMC transcription. The aim of this work was to analyze whether cFos directly interacts with the POMC gene in basal and corticotropin-releasing hormone (CRH) stimulated cells. Using progressively deleted POMC promoter sequences or ...
Winsky-Sommerer, R, Yamanaka, A, Diano, S, Borok, E, Roberts, AJ, Sakurai, T, Kilduff, TS, Horvath, TL and de Lecea, L (2004) Interaction between the corticotropin-releasing factor system and hypocretins (Orexins): A novel circuit mediating stress response ...
TY - JOUR. T1 - Arginine vasopressin is a much more potent stimulus to acth release from ovine anterior pituitary cells than ovine corticotropin-releasing factor. T2 - 1. In vitro studies. AU - Familari, Mlary. AU - Smith, A. Ian. AU - Smith, Robin. AU - Funder, John W.. PY - 1989/1/1. Y1 - 1989/1/1. N2 - Cultured rat and ovine anterior pituitary cells were treated with a range of doses (0.01-1,000 nM) of arginine vasopressin (AVP) and ovine corticotropin-releasing factor (CRF), alone or in combination, and medium and cell content of immuno-reactive (ir-)ACTH determined. In rat cells, a dose-response curve to CRF was obtained, with a threshold dose of 0.1 nM\ A VP was much less effective alone, but augmented CRF responses when administered with CRF. In ovine pituitary cells AVP markedly stimulated ACTH release in a dose-dependent fashion, and with a threshold of 0.1 nM\ in contrast, CRF increased ACTH release over basal only at doses , 100 nM. In combination, subthreshold doses of AVP ...
TY - JOUR. T1 - Vitamin D and corticotropin-releasing hormone in term and preterm birth. T2 - potential contributions to preterm labor and birth outcome. AU - Mohamed, Sara A.. AU - El Andaloussi, Abdeljabar. AU - Al-Hendy, Ayman. AU - Menon, Ramkumar. AU - Behnia, Faranak. AU - Schulkin, Jay. AU - Power, Michael L.. N1 - Funding Information: Partial support provided by grant UA6MC19010 from the Maternal Child Health Bureau of the Health Resources and Services Administration (HRSA). HRSA had no involvement in the planning, analysis, or write up for this research. Publisher Copyright: © 2017, © 2017 Informa UK Limited, trading as Taylor & Francis Group. Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 2018/11/2. Y1 - 2018/11/2. N2 - Background: Poor maternal vitamin D status and elevated circulating corticotropin-releasing hormone (CRH) are associated with preterm birth. It is not known if these risk factors are independent or interrelated. Both are associated with ...
This is the first study confirming that exogenous CRH can produce considerable changes in phasic contractions in human colon and small intestine. CRH is a peptide containing 41 amino acids,21distributed in the whole brain with dense localisation in the paraventricular nucleus of the hypothalamus,22 and now considered to be a major mediator of the stress response.10 Stress releases CRH from the paraventricular nucleus and CRH stimulates pituitary ACTH secretion.23Growing evidence from animal experiments indicates that endogenous CRH plays a role in mediating stress induced alteration of gastrointestinal motor function.6-9 Intracerebroventricular administration of CRH mimics the effects of various stressors in inhibiting small intestinal transit and stimulating colonic motor function through autonomic pathways in rats.6-9 Stress induced alterations in gastrointestinal motility in animals are abolished by intracerebroventricular administration of the CRH antagonist, α helical CRH9-41.6-9 Our data ...
The human CRH test (hCRH test) is used to differentiate Cushings disease (CD) from ectopic ACTH secretion (EAS); to assess autonomous cortisol secretion by the adrenal glands; to characterize pseudo-Cushings syndrome (CS) or adrenal insufficiency (AI).We measured ACTH and cortisol levels; we collected the peak values (peak ACTH and peak cortisol), and calculated the percentage increases (∆% ACTH and ∆% cortisol) after an iv. bolus of 100 μg hCRH.cross-sectional study of using hCRH tests from 2010 to 2019.Referral University-Hospital center.We enrolled 200 patients: 86 CD, 15 EAS, 18 adrenal CS, 25 mild adrenal autonomous cortisol secretion, 31 pseudo-CS, 25 suspected assess the diagnostic accuracy of hCRH test.The hCRH test was performed mainly for the differential diagnosis of ACTH-dependent CS or adrenal lesions (p=0.048). Peak ACTH and peak cortisol were higher in CD, and ∆% ACTH and ∆% cortisol were able to differentiate CD from EAS with a sensitivity and specificity ,80%. ...
TY - JOUR. T1 - Effect of alpha-helical CRH on quantitative electroencephalogram in patients with irritable bowel syndrome. AU - Tayama, J.. AU - Sagami, Y.. AU - Shimada, Y.. AU - Hongo, M.. AU - Fukudo, S.. PY - 2007/6/1. Y1 - 2007/6/1. N2 - Patients with irritable bowel syndrome (IBS) may have a higher tone of corticotropin-releasing hormone (CRH) in the brain. We tested our hypothesis that peripheral administration of CRH antagonist, α-helical CRH 9-41 (αhCRH), improves decreased alpha power spectra and increased beta power spectra of electroencephalogram (EEG) in IBS patients. A barostat bag was inserted to the descending colon of 10 normal controls and 10 IBS patients. The EEG power spectra and topography were measured during baseline period and colonic distention period with the administration of saline followed by the administration of 10 μg kg-1 of αhCRH. IBS patients showed a significantly lower alpha power percentage and a higher beta power percentage than normal controls during ...
Neuropeptides such as neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) have been implicated not only in acute regulation of stress/anxiety-related behaviors, but adaptations and changes in these neuropeptide systems may also participate in the regulation of behavior and endocrine responses during chronic stress. NPY is an endogenous anxiolytic neuropeptide, while CRH has anxiogenic properties upon central administration. Changes in these neuropeptide systems may contribute to disease states and give us indications for putative treatment targets for stress/anxiety disorders as well as alcohol/drug dependence. In this review, we briefly present these two systems and review their involvement in mediating the responses to acute and chronic stressors, as well as their possible roles in the development and progression of stress/anxiety disorders. We suggest that neuropeptides may be attractive in treatment development for stress/anxiety disorders, as well as for alcohol/drug dependence, ...
TY - JOUR. T1 - Effect of betamethasone in vivo on placental corticotropin-releasing hormone in human pregnancy. AU - Marinoni, E. AU - Korebrits, C. AU - Di Iorio, R. AU - Cosmi, EV. AU - Challis, John. PY - 1998. Y1 - 1998. U2 - 10.1016/S0002-9378(98)70490-9. DO - 10.1016/S0002-9378(98)70490-9. M3 - Article. VL - 178. SP - 770. EP - 778. JO - American Journal of Obstetrics & Gynecology. JF - American Journal of Obstetrics & Gynecology. SN - 0002-9378. IS - 4. ER - ...
TY - JOUR. T1 - CRH receptor antagonists. T2 - Advances and prospective. AU - Ayala, A. R.. AU - Wand, G. S.. PY - 2000/1/1. Y1 - 2000/1/1. N2 - Corticotrophin releasing hormone (CRH), a 41-amino acid peptide, is the main regulator of pituitary adrenocorticotrophic hormone (ACTH). Its secretion in humans plays a major role in the physiologic response to stress. CRH Type 1 and 2 receptors are widely distributed throughout the CNS and to a lesser extent in peripheral tissues. The CRH neurones modulate autonomic (locus ceruleus) and limbic system function. Furthermore, the presence of CRH receptors in inflammatory tissue and the placenta suggests that this neuropeptide is involved in modulation of the immune response and parturition. Hypersecretion of CRH is thought to play a pivotal role in the pathophysiology of major depression, anxiety and drug withdrawal. Therefore, antagonising CRH action has become a major therapeutic strategy for these disorders. Data from transgenic mice lacking or ...
Corticotropin-releasing factor (CRF) is typically considered to mediate aversive aspects of stress, fear and anxiety. However, CRF release in the brain is also elicited by natural rewards and incentive cues, raising the possibility that some CRF systems in the brain mediate an independent function of positive incentive motivation, such as amplifying incentive salience. Here we asked whether activation of a limbic CRF subsystem magnifies the increase in positive motivation for reward elicited by incentive cues previously associated with that reward, in a way that might exacerbate cue-triggered binge pursuit of food or other incentives? We assessed the impact of CRF microinjections into the medial shell of nucleus accumbens using a pure incentive version of Pavlovian-Instrumental transfer, a measure specifically sensitive to the incentive salience of reward cues (which it separates from influences of aversive stress, stress reduction, frustration and other traditional explanations for stress-increased
Background Peripheral corticotrophin-releasing factor (CRF) plays an important role in stress-induced alterations of gastrointestinal motility. CRF injected peripherally inhibits gastric emptying, but its effect on gastric contractions has not bee
Centrally released oxytocin (OXT) has anxiolytic and anti-stress effects. Delayed gastric emptying (GE) induced by acute restraint stress (ARS) for 90 min is completely restored following 5 consecutive days of chronic homotypic restraint stress (CHS), via up-regulating hypothalamic OXT expression in rats. However, the mechanism behind the restoration of delayed GE following CHS remains unclear. Gamma-aminobutyric acid (GABA)-projecting neurons in the paraventricular nucleus (PVN) have been shown to inhibit corticotropin releasing factor (CRF) synthesis via GABA(A) receptors. We hypothesized that GABA(A) receptors are involved in mediating the inhibitory effect of OXT on CRF expression in the PVN, which in turn restores delayed GE following CHS. OXT (0.5 μg) and selective GABA(A) receptor antagonist, bicuculline methiodide (BMI) (100 ng), were administered intracerebroventricularly (icv). Solid GE was measured under non-stressed (NS), ARS and CHS conditions. Expression of CRF mRNA in the PVN was ...
Introduction: Marchigian Sardinian alcohol-preferring (msP) rats exhibit innate preference for alcohol along with anxious phenotype. In these animals, two single-nucleotide polymorphisms in position -1,836 and -2,097 from the first start codon of the CRF1-R transcript have been found. Materials and Methods: Here, we examined whether these point mutations account for the heightened anxiety-like behavior and stress responsiveness of msP rats. We rederived the msP rats to obtain two distinct lines carrying the wild-type (GG) and point mutations (AA), respectively. Results: CRF1-R gene expression analysis revealed significant dysregulation of the system in the extended amygdala of AA rats. At the behavioral level, using the elevated plus maze, we found that both AA and GG lines had higher basal anxiety compared to Wistar rats. In the defensive burying test, AA rats showed decreased burying behavior compared to the GG and the unselected Wistar lines. Freezing/immobility did not differ among AA and GG ...
Drug addiction can be defined by a three-stage cycle-binge/intoxication, withdrawal/negative affect, and preoccupation/anticipation-that involves allostatic changes in the brain reward and stress systems. Two primary sources of reinforcement, positive and negative reinforcement, have been hypothesized to play a role in this allostatic process. The negative emotional state that drives negative reinforcement is hypothesized to derive from dysregulation of key neurochemical elements involved in the brain reward and stress systems. Specific neurochemical elements in these structures include not only decreases in reward system function (within-system opponent processes) but also recruitment of the brain stress systems mediated by corticotropin-releasing factor (CRF) and dynorphin-κ opioid systems in the ventral striatum, extended amygdala, and frontal cortex (both between-system opponent processes). CRF antagonists block anxiety-like responses associated with withdrawal, block increases in reward thresholds
The purpose of this study is to examine the safety and efficacy of XERECEPT (human Corticotropin-Releasing Factor, or hCRF) compared to dexamethasone in
Supplementary Materials1. just correlated with ER favorably, but with ErbB3 in clinical breasts cancers datasets inversely. LRIG1, an estrogen-inducible ErbB down-regulator, was reduced in a -panel of fulvestrant-treated luminal breasts cancers cells. Ectopic LRIG1 appearance from an estrogen-independent promoter uncoupled LRIG1 from estrogen legislation, sustaining LRIG1 and preserving low ErbB3 amounts in fulvestrant-treated cells thus. An LRIG1 mutant missing the ErbB3 relationship motif was inadequate to down-regulate ErbB3. Significantly, LRIG1 overexpression improved fulvestrant-mediated development inhibition, while cells expressing the LRIG1 mutant had been delicate to fulvestrant badly, despite effective ER down-regulation. In keeping with these total outcomes, LRIG1 appearance correlated favorably with an increase BF 227 of disease-free success in anti-estrogen-treated breasts cancers sufferers. These data suggest that ER-dependent expression of LRIG1 dampens ErbB3 signaling in luminal ...
Background CCR5 is a CC chemokine receptor mixed up in migration of effector leukocytes including macrophages, NK, and T cells into inflamed tissue. IL-17+Compact disc4+…. Continue reading Background CCR5 is a CC chemokine receptor mixed up in migration. Comments closed ...
Many unmet needs persist around adrenal insufficiency [132, 133]. Adrenal glands are called the gland of stress. They are made of two distinct tissues: 1) the central medulla derives from the neuro-ectoderm and produces catecholamines; 2) the cortex derives from the intermediate mesoderm and is characterised by its activity of steroidogenesis [134]. Progenitor cells are found within the mesenchymal capsule and are embedded in the outermost cortical zone. The cortex is divided into three distinct zones. The outer zona glomerulosa produces mineralocorticoids (aldosterone), the zona fasciculata produces GCs (cortisol) and the zona reticularis produces adrenal androgens (dihydroepiandrosterone). GC production is stimulated by adrenocorticotropic hormone (ACTH) within a well-known negative feedback loop orchestrated by the pituitary gland, in response to hypothalamic corticotropin-releasing hormone release. Both ACTH and GC releases are cyclic, with a zenith in the morning and nadir in the middle ...
We acknowledge the Gadigal people of the Eora Nation, the traditional owners and custodians of the land on which the Garvan Institute of Medical Research is located. We pay respects to Elders, past, present and future, and recognise the continuing connection and contribution to this land. ...
Stressful stimuli induced by immobilization are perceived as acute stress in rats. This acute stress activates corticotropin-releasing hormone (CRH) neurons in the hypothalamic paraventricular nucleus (PVN), resulting in stimulation of the hypothalamic-pituitary-adrenal (HPA) axis. The ventral ascending noradrenergic bundles (V-NAB) from the brainstem innervate the PVN. To investigate the relationship between the response of the HPA axis and the V-NAB, we examined changes in plasma corticosterone, the final output of the HPA axis, and extracellular noradrenaline (NA) in the PVN following immobilization stress in rats that received bilateral 6-hydroxydopamine (6-OHDA) lesions of the V-NAB. 6-OHDA microinjection into the V-NAB reduced the magnitude of the responses of plasma corticosterone and extracellular NA in the PVN following immobilization stress. Our results suggest that V-NAB innervation of the PVN is involved in immobilization stress-induced activation of the HPA axis.
Optimization of 3-phenylpyrazolo[1,5-a[pyrimidines as potent corticotropin-releasing factor-1 antagonists with adequate lipophilicity and water solubility ...
Corticotropin-releasing factor (CRF) and urotensin I (UI) precursor cDNAs were cloned and sequenced from a goldfish brain cDNA library in order to investigate the distribution of CRF and UI mRNAs in goldfish brain and the regulation of CRF and UI gene expression. The CRF (966-bp) and UI (769-bp) cDNAs encode 163- and 146-amino acid precursors, respectively, and consist of a signal peptide sequence, a cryptic region, and a 41-amino acid mature peptide at the carboxy terminal. The deduced amino acid sequences of the CRF and UI peptides exhibit a sequence identity of 54%. Northern blot analysis revealed a single size of CRF (1.3 kb) and UI (2.0 kb) mRNAs, which are expressed in the telencephalon-preoptic, hypothalamic, optic tectum-thalamus, and posterior brain regions, but not in the pituitary. In addition, while the CRF gene is strongly expressed in the olfactory bulbs, the UI gene is not. In brain regions in which both genes are expressed, the mRNA levels of CRF were three- to sevenfold higher ...
We administered corticosterone to wild-type and Pomc−/− mice for 10 days, achieving comparable plasma corticosterone and hypothalamic CRH expression levels. Only in the Pomc−/− mice did this cause increased body weight and fat mass. An increase in food intake was also only seen in Pomc-null mice, with this exacerbation of preexisting hyperphagia likely to be as a result of a corticosterone-dependent increase in the expression of the orexigenic neuropeptide, AgRP.. Ten days of glucocorticoid treatment did not increase blood glucose levels but did increase plasma insulin levels in both wild-type and Pomc−/− mice. However, the absolute plasma insulin levels measured and fold increase from control were markedly higher in Pomc-null mice. Furthermore, corticosterone treatment to mice from weaning resulted in a progressive rise in blood glucose and frank diabetes by 10-12 weeks only in Pomc−/− mice, having no such effect in wild-type animals.. Two other groups have investigated the ...
Supplementary MaterialsAdditional file 1: Physique S1. Microglia are the primary ROS-producing cells in Tfpi the CNS in response to trauma. Given that they possess the necessary machinery to incorporate iron under basal and LPS-stimulated conditions (Additional?file?1: Determine S1), we examined the effect of iron on microglial ROS production. Primary rat microglia cultures were exposed to the Fe2+ donor, FeSO4, LPS, or both for 24?h. We detected a significant ROS accentuation among the cells with FeSO4 exposure that was similar to LPS exposure (Ctrl vs. FeSO4, em p /em ?=?0.0027; Ctrl vs. LPS, em p /em ?=?0.0023, one-way ANOVA with Tukeys post-hoc test, Fig.?1a). Combining FeSO4 with LPS for 24?h resulted in a significant elevation of ROS release in comparison to either FeSO4 or LPS alone (FeSO4 vs FeSO4?+?LPS, em p /em ? ?0.0001; LPS vs FeSO4?+?LPS, em p /em ? ?0.0001, one-way ANOVA with Tukeys post-hoc test, Fig.?1a). Further, administration of the iron chelating agent DFO resulted in ...
Data Availability StatementAll data comes in the manuscript. was extensively investigated for recurrent pulmonary infections and irregular radiological findings, which included pulmonary nodules, infiltrates and splenomegaly. Subsequently, she was referred to an immunology medical center, where immunoglobulin alternative treatment was started for what was ultimately considered to be CVID. Shortly afterwards, evaluation of her medical, radiological and histological findings at a specialist interstitial lung disease medical center led to a analysis of GLILD. Conclusion CVID is definitely a condition which should become suspected in individuals with immunodeficiency and recurrent infections. Concomitant autoimmune disorders such as AL082D06 haemolytic anaemia and immune thrombocytopenia may further support the analysis. As illustrated within this complete case, theres a uncommon association between CVID and inflammatory participation from the neurological program. Respiratory physicians also needs ...
The flight or fright response, also known as acute stress response, is a survival mechanism that allows individuals to react promptly to a life-threatening situation. The limbic system plays a pivotal role in controlling such behavior.. Neural signals arising from any stressful situation activate the amygdala, which subsequently processes the information and activates the hypothalamus. Afterward, the hypothalamus sends sympathetic discharges to the adrenal gland and facilitates the release of adrenalin into blood. This in turn activates various autonomic responses to trigger the flight or fright response.. After the initial adrenalin surge, the hypothalamus activates the hypothalamic-pituitary-adrenal axis to suppress the sympathetic discharge. In case of persistent stressful condition, the hypothalamus secretes corticotropin-releasing hormone and activates the pituitary gland to release adrenocorticotropic hormone.. This hormone activates the adrenal gland and facilitates the secretion of ...
Verucerfont is a corticotropin-releasing factor receptor 1 (CRF1) antagonist with IC50s of ~6.1, >1000 and >1000 nM for CRF1, CRF2, and CRF-BP, respectively. Buy Verucerfont (GSK561679) from AbMole BioScience.
Brain, Corticotropin, Corticotropin-releasing Factor, Crf Receptor, Gastric Emptying, Norepinephrine, Neurons, Neuropeptide, Mice, Anxiety, and Hydrogen
A non-peptide, kappa-opioid receptor agonist which has also been found to stimulate the release of adrenocorticotropin (ADRENOCORTICOTROPIC HORMONE) via the release of hypothalamic arginine vasopressin (ARGININE VASOPRESSIN) and CORTICOTROPIN-RELEASING HORMONE. (From J Pharmacol Exp Ther 1997;280(1):416-21) . ...
A non-peptide, kappa-opioid receptor agonist which has also been found to stimulate the release of adrenocorticotropin (ADRENOCORTICOTROPIC HORMONE) via the release of hypothalamic arginine vasopressin (ARGININE VASOPRESSIN) and CORTICOTROPIN-RELEASING HORMONE. (From J Pharmacol Exp Ther 1997;280(1):416-21) . ...
Two populations of neurons in the paraventricular nucleus of the hypothalamus that have different efferent projections and physiological roles in the regulation of visceral responses were characterized morphologically with a combined intracellular filling, retrograde tracer, and immunohistochemical method. Neuroendocrine cells were retrogradely labeled by an intravenous injection of Fast blue, and distinguished from descending neurons that were retrogradely labeled by an injection of fluorogold into the spinal cord. Retrogradely labeled neurons were selectively penetrated and filled intracellularly with Lucifer yellow to visualize detailed features of their morphology. Corticotropin-releasing hormone (CRH)-containing neurons were distinguished from other neuroendocrine cells by immunostaining the tissue with an antiserum to rat CRH. Morphometric features of defined populations of neurons were then quantified and reconstructed graphically to generate multicellular montage drawings that ...
The effect of NmU on stress and pain perception pathways has been demonstrated using mice. In contrast to NmU peptide-deficient mice, NmUR2 knockout (KO) mice appeared normal with regard to stress, anxiety, body weight regulation, and food consumption. However, the NmUR2 KO mice exhibit reduced pain sensitivity in both hot plate test and the chronic phase of the formalin test. Furthermore, facilitated excitatory synaptic transmission in spinal dorsal horn neurons, a mechanism by which NmU stimulates pain, did not occur in NmUR2 KO mice. Both NmUR2 expression and NmU-23 binding sites are highly localized to the outer layers of the spinal dorsal horn, and administration of NmU via intracerebroventricular (ICV) injections usually increases pain sensitivity in rats and mice. The expression of NmUR2 in the paraventricular nucleus of hypothalamus (PVN), a major site for the release of Corticotropin-releasing hormone (CRH), suggests an alternative role in mediating stress response. NmU and its ...
The encoded protein is a secreted calcium-binding protein which is found in the cytoplasm. It is related to calbindin D-28K and calretinin. This protein is thought to be involved in potassium chloride-stimulated calcium flux and cell proliferation.[6] This protein plays an important role in the release of the stress hormone Corticotropin-releasing hormone (CRH) and which only then enables stress processes in the brain. ...
Nervous System (CNS) may have an important role in CFS. One of the biggest overlooked factors in CFS is broad- Physical or emotional stress alters the activity of the spectrum nutritional deficiency. Many people mistakenly Hypothalamus-Pituitary Axis (HPA), leading to altered release assume that if you eat a well-balanced diet, you will get all the of corticotrophin-releasing hormone (CRH), cortisol and other nutrients that you need, yet scientific studies have shown hormones. CRH influences the immune system and many other body systems, and may also affect several aspects of recommending nutritional supplementation. In an expert review of vitamins for disease prevention published in the highly prestigious Journal of the American Medical Recent studies have shown that CFS patients often produce Association it was concluded that; Most people do not lower levels of cortisol than do healthy controls.7 Cortisol consume an optimal amount of all vitamins by diet alone. suppresses inflammation and ...
Management of advanced stages requires excision. Drug therapy of insomnia. Predominantly medullary stimulants, e.G. High or moderate) 0.3 (0.1 0.5) 2% (1.7 8.10%) follow each row from left to right to see how each symptom alters the probability of cancer triage result likelihood ratio probability probability ratio probability. Control over the acromioclavicular joint rather than direct perception. Even a slight rise in blood glucose, hence. Ideomotor aphasia n. An approach to decrease testosterone levels following consumption). So far, there is violent fall without loss of ambulation. Thus, cox-1 is physiological and pathological abnormality present in yeast, vegetables and fruits. See corticotrophin-releasing hormone, growth hormone (the fountain of youth + phren mind, originally midriff, the supposed seat of power in response to colchicine and nsaid. Their presence in the retina as containing two different languages, and forms cyanmethemoglobin, a relatively small displacement of the autonomic ...
rs242941 is a SNP in the corticotrophin-releasing hormone receptor 1 CRHR1 gene. [PMID 19210659] (G;G) better response to inhaled corticosteroids fluticasone propionate and salmeterol in patients with COPD in a Korean study with 84 subjects. ...
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Antalarmin je lek koji deluje kao antagonist kortikotropin-oslobađajućeg hormonskog receptora 1. Kortikotropin-oslobađajući faktor (CRF), takođe poznat kao kortikotropin-oslobađajući hormon, je endogeni peptidni hormon oslobođen u responsu na razne stimuluse kao što su hronični stres i adikcija na droge. To zatim inicira oslobađanje kortikotropina (ACTH), hormona koji učestvuje u fiziološkom responsu na stres. Smatra se da hronično oslobađanje CRF i ACTH hormona direktno ili indirektno učestvuje u mnogim štetnim fiziološkim efektima hroničnog stresa, kao što su eksesivno oslobađanje glukokortikoida, dijabetes melitus, osteoporoza, čir na dvanaestopalačnom crevu, anksioznost, depresija, i razvoj visokog krvnog pritiska i konsekventni kardiovaskularni problemi.[1] Antalarmin je nepeptidni lek koji blokira CRF-1 receptor, i kao posledica toga, umanjuje oslobađanje ACTH-a u responsu na hronični stres.[2] Na životinjskim studijama je pokazano da redukuje response na stresne ...
This demonstration is achieved based on the technical merit in our transgenic mice, in which the transgene expression is inducible/reversible. The time resolution for this inducible/reversible feature is within 1 week, which is high enough for this time-coupling analysis. However, it is still not clear how this real-time coupling occurs, partially due to the fact that the functional significance of the CCKergic system is still not fully understood. As G protein-coupled receptors, CCKR are associated with Ca2+ release, PKC activation, PLA2 activity, and cAMP production [120]. As stress, either real or imaged, is a necessary inducer for ADs, the CRF/HPA system must play a unique role in anxiety-related behaviors. Indeed, a huge body of evidence has documented this notion. For example, administration of CRF [70-72] or CRFR1 agonists [69,73,74] or overexpression of the CRF gene [75-77] produces Anxiety-like behaviors (ALBs) in the animals. On the other hand, CRFR1 antagonists exert significantly ...
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C, B, CRF01_AE, A, G, CRF02_AG, D, CRF06_cpx, F, CRF07_BC, CRF45_cpx, CRF18_cpx, CRF09_cpx, CRF10_CD, G + CRF02_AG, B + CRF01_AE, CRF11_cpx, CRF12_BF, CRF49_cpx, A + G ...
If secondary adrenal insufficiency is diagnosed, the insulin tolerance test (ITT) or the CRH (corticotropin-releasing hormone) ... a progestogen steroid hormone related to progesterone Luteinizing hormone - a pituitary hormone that stimulates sex hormone ... "Corticotropin-releasing hormone stimulation test". Cite journal requires ,journal= (help) unknown. "Role of ACTH in Regulation ... ACTH is a hormone produced in the anterior pituitary gland that stimulates the adrenal glands to release cortisol, ...
... of the hypothalamus releases corticotropin-releasing hormone (CRH), which stimulates the pituitary gland to release ... Corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism). This causes the blood ACTH levels to be elevated ... "Cushing's syndrome secondary to ectopic corticotropin-releasing hormone-adrenocorticotropin secretion". The Journal of Clinical ... "Hypothalamic hamartoma secreting corticotropin-releasing hormone. Case report". Journal of Neurosurgery. 100 (2 Suppl ...
"Hypothalamic hamartoma secreting corticotropin-releasing hormone. Case report". J Neurosurg. 100 (2 Suppl Pediatrics): 212-6. ... Mahachoklertwattana P, Kaplan SL, Grumbach MM (July 1993). "The luteinizing hormone-releasing hormone-secreting hypothalamic ... "Treatment of gonadotropin dependent precocious puberty due to hypothalamic hamartoma with gonadotropin releasing hormone ... Hormonal suppressive therapy with luteinizing hormone receptor agonists like leuprorelin can be used to treat the seizure ...
"Corticotropin-releasing hormone as adrenal androgen secretagogue". Pediatric Research. 46 (3): 351-3. doi:10.1203/00006450- ... Instead, they are released into the blood stream and taken up in the testis and ovaries to produce testosterone and the ...
Corticotropin-releasing factor (CRF), also known as corticotropin-releasing hormone, is an endogenous peptide hormone which is ... This then triggers the release of corticotropin (ACTH), another hormone which is involved in the physiological response to ... Corticotropin releasing hormone antagonists Antalarmin CP-154,526 Emicerfont Verucerfont "International Nonproprietary Names ... Zoumakis E, Rice KC, Gold PW, Chrousos GP (November 2006). "Potential uses of corticotropin-releasing hormone antagonists". ...
It belongs to corticotropin-releasing hormone binding protein family. Corticotropin-releasing hormone is a potent stimulator of ... "Entrez Gene: CRHBP corticotropin releasing hormone binding protein". Human CRHBP genome location and CRHBP gene details page in ... 2003). "The corticotropin-releasing hormone binding protein is associated with major depression in a population from Northern ... 1995). "Mapping the human corticotropin releasing hormone binding protein gene (CRHBP) to the long arm of chromosome 5 (5q11.2- ...
Corticotropin-releasing hormone (CRH) is activated by the HPA axis during times of stress. Heightened CRH levels have been ... Hypothalamic pituitary adrenal axis and corticotropin-releasing hormone. The hypothalamic pituitary adrenal (HPA) axis is ...
It belongs to the corticotropin-releasing hormone family. This gene is a member of the sauvagine/corticotropin-releasing factor ... "Corticotropin-releasing hormone system in human adipose tissue". The Journal of Clinical Endocrinology and Metabolism. 89 (2): ... "Human stresscopin and stresscopin-related peptide are selective ligands for the type 2 corticotropin-releasing hormone receptor ... It is structurally related to the corticotropin-releasing factor (CRF) gene and the encoded product is an endogenous ligand for ...
... but not corticotropin-releasing hormone". The Journal of Clinical Endocrinology and Metabolism. 83 (2): 708-11. doi:10.1210/jc. ... "Human stresscopin and stresscopin-related peptide are selective ligands for the type 2 corticotropin-releasing hormone receptor ... Morin SM, Ling N, Liu XJ, Kahl SD, Gehlert DR (1999). "Differential distribution of urocortin- and corticotropin-releasing ... Lim MM, Tsivkovskaia NO, Bai Y, Young LJ, Ryabinin AE (2006-01-01). "Distribution of corticotropin-releasing factor and ...
Corticotropin-releasing hormone (CRH), also known as Corticotropin-releasing factor, is an endogenous peptide hormone released ... a nonpeptide corticotropin-releasing hormone (CRH) receptor antagonist: suppression of pituitary ACTH release and peripheral ... CP-154,526 Pexacerfont Corticotropin-releasing hormone antagonist Zoumakis E, Rice KC, Gold PW, Chrousos GP (November 2006). " ... June 2002). "Corticotropin releasing hormone (CRH) antagonist attenuates adjuvant induced arthritis: role of CRH in peripheral ...
April 2005). "Corticotropin-releasing hormone activates ERK1/2 MAPK in specific brain areas". Proceedings of the National ...
Florio P, Zatelli MC, Reis FM, degli Uberti EC, Petraglia F (2007). "Corticotropin releasing hormone: a diagnostic marker for ... GH and TSH in response to hypothalamic releasing factors. These effects on HPA hormone levels may be beneficial for some ... has also been shown to elevate ACTH independently from CRH levels and to amplify the release of other HPA axis hormones such as ... Cavun S, Savci V (Oct 2004). "CDP-choline increases plasma ACTH and potentiates the stimulated release of GH, TSH and LH: the ...
It is a synthetic form of human corticotropin-releasing hormone (hCRH). The corticorelin stimulation test helps to ... June 1994). "General pharmacological properties of the human corticotropin-releasing hormone corticorelin (human)". ... differentiate between the causes for adrenocorticotropic hormone (ACTH)-dependent hypercortisolism. It is used to distinguish a ...
Fukudo S (January 2007). "Role of corticotropin-releasing hormone in irritable bowel syndrome and intestinal inflammation". ... Evidence has demonstrated that the release of high levels of proinflammatory cytokines during acute enteric infection causes ... "New Studies Examine the Evidence on Probiotics in IBS" (PDF) (Press release). American College of Gastroenterology. October 31 ...
Colocalization of connexin 36 and corticotropin-releasing hormone in the mouse brain. BMC Neuroscience 10:41. "Lisa Gunaydin, ...
Papadopoulou N, Kalogeromitros D, Staurianeas NG, Tiblalexi D, Theoharides TC (November 2005). "Corticotropin-releasing hormone ... Finally, PLP re-forms its original Schiff base at lysine 305, and histamine is released. This mechanism is very similar to ... H3 controls histamine turnover by feedback inhibition of histamine synthesis and release. Finally, H4 plays roles in mast cell ...
These hormones include dopamine, norpinephrine, thyrotropin-releasing hormone, and corticotropin-releasing hormone. Many of ... The somatostatin hormone itself can negatively affect the uptake of hormones in the body and may play a role in some hormonal ... GRCh38: Ensembl release 89: ENSG00000180616 - Ensembl, May 2017 GRCm38: Ensembl release 89: ENSMUSG00000047904 - Ensembl, May ... and also acts as an inhibitor to the milk producing hormone in female mammals, prolactin, and growth hormones. Researchers ...
Release of corticotropin-releasing hormone (CRH) from the hypothalamus is influenced by stress. CRH is a major regulator of the ... Glucocorticoids also inhibit the further secretion of corticotropin-releasing hormone from the hypothalamus and ACTH from the ... Hypothalamic Pituitary Adrenal axis releases the needed hormones to support the immune system. Activity of the immune system is ... facilitate inflammation through induction of signaling pathways and through activation of the Corticotropin-releasing hormone. ...
Another possibility being researched is a hyper-production of the Corticotropin-releasing hormone (CRH). It is possible that ... Therapies with hormones is the standard of care, namely adrenocorticotrophic hormone (ACTH), or oral corticosteroids such as ...
The secretion of corticotropin-releasing hormone by the hypothalamus triggers cells in the neighboring anterior pituitary to ... ACTH is in turn controlled by the hypothalamic peptide corticotropin-releasing hormone (CRH), which is under nervous control. ... Minton JE, Parsons KM (March 1993). "Adrenocorticotropic hormone and cortisol response to corticotropin-releasing factor and ... forcing the secretion of corticotropin-releasing hormone, thus antagonizing IL-1). The suppressor cells are not affected by ...
One study found that the stress hormone placental corticotropin-releasing hormone (pCRH) mediated the relationship between ... Hahn-Holbrook J, Schetter CD, Arora C, Hobel CJ (July 2013). "Placental Corticotropin-Releasing Hormone Mediates the ...
... as well as blocking the Y1-mediated corticotropin releasing hormone release. It has also been used as a lead compound to ... "Involvement of neuropeptide Y Y1 receptors in the regulation of neuroendocrine corticotropin-releasing hormone neuronal ...
Additionally, arginine vasopressin upregulates corticotropin-releasing hormone (CRH), which is a hormone important for stress ... A common pathway dysregulated in HPA axis involves a hormone known as glucocorticoid and its receptor, which aid in stress ... Offspring of these mice had increased anxiety in response to stressful conditions, increased stress hormone levels, ... and higher levels of the stress hormone cortisol. The effect of parental exposure to stress has been tested experimentally as ...
Carter's research focuses on neuropeptide and steroid hormones, including oxytocin, vasopressin, corticotropin-releasing ... 2002) The neurobiology of social affiliation and pair bonding, In Hormones, Brain and Behavior, edited by D. Pfaff, pp. 299-337 ... and implicated these hormones in the regulation of long-lasting neural and effects of early social experiences. She also has a ... vasopressin and hormones of the hypothalamic-pituitary-adrenal ("stress") axis in the traits of monogamy including pair-bond ...
"Association of a corticotropin-releasing hormone receptor 1 haplotype and antidepressant treatment response in Mexican- ... "Modulation of pancreatic islets-stress axis by hypothalamic releasing hormones and 11beta-hydroxysteroid dehydrogenase". ... luteinizing hormone, and estradiol in healthy women". Proceedings of the National Academy of Sciences of the United States of ...
"Human stresscopin and stresscopin-related peptide are selective ligands for the type 2 corticotropin-releasing hormone receptor ... potential role of the type-2 corticotropin-releasing hormone receptor in the control of myometrial contractility". ... This gene is a member of the sauvagine/corticotropin-releasing factor/urotensin I family. It is structurally related to the ... 2001). "Urocortin II: a member of the corticotropin-releasing factor (CRF) neuropeptide family that is selectively bound by ...
... it exerts similar physiological effects as corticotropin-releasing hormone. Sauvagine belongs to the corticotropin-releasing ... Sauvagine has been shown to interact with corticotropin releasing factor receptors 1 and 2, and (as with other CRF-related ... Sauvagine is a neuropeptide from the corticotropin-releasing factor (CRF) family of peptides and is orthologous to the ... Lovejoy DA, de Lannoy L (December 2013). "Evolution and phylogeny of the corticotropin-releasing factor (CRF) family of ...
... as well as raises levels of placental corticotropin-releasing hormone (CRH) which can lead to preterm labor. These findings can ... Growth hormone (GH) therapy at a certain dose induced catch-up of lean body mass (LBM). However percentage body fat decreased ... "GH Treatment Effects on Body Composition in SGA". Growth, Genetics & Hormones. 24 (1). May 2008.[permanent dead link] "Low ... Stress causes the body to produce stress hormones called glucocorticoids that can suppress the immune system., ...
Hormones which have been studied include estrogen, progesterone, thyroid hormone, testosterone, corticotropin releasing hormone ... Some studies show that hormone therapy may be effective in women with PPD, supported by the idea that the drop in estrogen and ... Aberrant steroid hormone-dependent regulation of neuronal calcium influx via extracellular matrix proteins and membrane ... Soares CN, Zitek B (July 2008). "Reproductive hormone sensitivity and risk for depression across the female life cycle: a ...
Two genes of interest are CHRH1 (corticotropin-releasing hormone receptor 1) and TBX21 (transcription factor T-bet). Both genes ... and Philip Showalter Hench were awarded the Nobel Prize for Physiology and Medicine in 1950 for their work on hormones of the ... The cortico- part of the name refers to the adrenal cortex, which makes these steroid hormones. Thus a corticosteroid is a " ... Corticosteroids are a class of steroid hormones that are produced in the adrenal cortex of vertebrates, as well as the ...
... leptin and corticotropin-releasing hormone have all been shown to suppress food intake.[18][19] ... This hormone is thought to be a satiety signal to the brain. Peptide YY 3-36 is a hormone released by the small intestine and ... The signals from the stomach are initiated by the release of the peptide hormone ghrelin. Ghrelin is a hormone that increases ... The hormone cholecystokinin is secreted by the duodenum, and it controls the rate at which the stomach is emptied.[23] ...
Administration of corticotropin releasing hormone (CRH) can differentiate this condition from ectopic ACTH secretion. In a ... Any intermediate values need to be cautiously interpreted and a corticotropin-releasing hormone (CRH) test is advised in order ... corticotropin releasing hormone) (tertiary hypercortisolism/hypercorticism) that stimulates the synthesis of cortisol by the ... the tumor cells will be stimulated to release corticotropin and elevated plasma corticotropin levels will be detected.[7] This ...
It comprises corticotropin-releasing factor (CRF), released by the hypothalamus; adrenocorticotropic hormone (ACTH), released ... Schematic of the HPA axis (CRH, corticotropin-releasing hormone; ACTH, adrenocorticotropic hormone). ... Vasopressin can be thought of as "water conservation hormone" and is also known as "antidiuretic hormone." It is released when ... which contains neuroendocrine neurons that synthesize and secrete vasopressin and corticotropin-releasing hormone (CRH). These ...
Corticotropin-releasing hormone (1. *2). *EMR (1. *2. *3). *Glucagon (GR. *GIPR ... a b c GRCh38: Ensembl release 89: ENSG00000163251 - Ensembl, May 2017 *^ a b c GRCm38: Ensembl release 89: ENSMUSG00000045005 ...
2008). «Elevated midpregnancy corticotropin-releasing hormone is associated with prenatal, but not postpartum, maternal ...
... such as corticotropin-releasing factor, may be involved. Peripherally, the autonomic nervous system, especially the sympathetic ... and hormones (such as cortisol) which are implicated in anxiety. The epigenetic signature of at least one of these genes BDNF ...
... phenotypic variations of corticotropin releasing hormone (CRH) and arginine vasopressin (AVP), and down-regulation of adrenal ... Such treatment augmentations can include lithium pharmacology, thyroid hormone augmentation, amisulpride, buspirone, bupropion ...
Corticotropin releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... Bradykinin was to prove a new autopharmacological principle, i.e., a substance that is released in the body by a metabolic ... Bradykinin raises internal calcium levels in neocortical astrocytes causing them to release glutamate, though this finding has ... Bradykinin dilates blood vessels via the release of prostacyclin, nitric oxide, and Endothelium-Derived Hyperpolarizing Factor ...
Stimulation of the hypothalamic-pituitary-adrenal axis by stimulating the release of corticotropin releasing hormone (CRH) ... a b c GRCm38: Ensembl release 89: ENSMUSG00000024401 - Ensembl, May 2017 *^ "Human PubMed Reference:".. .mw-parser-output cite. ... In 1985, Bruce A. Beutler and Anthony Cerami discovered that cachectin (a hormone which induces cachexia) was actually TNF.[18] ... TNF can be produced ectopically in the setting of malignancy and parallels parathyroid hormone both in causing secondary ...
Corticotropin-releasing hormone (1. *2). *EMR (1. *2. *3). *Glucagon (GR. *GIPR ... a b c GRCh38: Ensembl release 89: ENSG00000186188 - Ensembl, May 2017 *^ a b c GRCm38: Ensembl release 89: ENSMUSG00000054200 ... hormone secretion. • negative regulation of apoptotic process. • response to peptide. • cellular response to hormone stimulus. ...
Corticotropin-releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... causing the formation of a puromycylated nascent chain and premature chain release.[2] The exact mechanism of action is unknown ...
Corticotropin-releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... a b c GRCh38: Ensembl release 89: ENSG00000167244 - Ensembl, May 2017 *^ a b c GRCm38: Ensembl release 89: ENSMUSG00000048583 ... together with luteinizing hormone (LH). Thus, IGF2 acts as a co-hormone together with both FSH and LH.[10] ... hormone activity. • GO:0001948 protein binding. • growth factor activity. • insulin-like growth factor receptor binding. • ...
Corticotropin-releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... Bradykinin is a peptide-based hormone that is formed locally in tissues, very often in response to a trauma. It increases ... "Jerini Receives European Commission Approval for Firazyr (Icatibant) in the Treatment of HAE" (Press release). Jerini AG. 15 ... "FDA Approves Shire's FIRAZYR (icatibant injection) for Acute Attacks of Hereditary Angioedema (HAE)" (Press release). Shire. ...
Corticotropin-releasing hormone (1. *2). *EMR (1. *2. *3). *Glucagon (GR. *GIPR ... a b c GRCh38: Ensembl release 89: ENSG00000171659 - Ensembl, May 2017 *^ a b c GRCm38: Ensembl release 89: ENSMUSG00000040229 ...
The majority of reports indicate people with PTSD have elevated levels of corticotropin-releasing hormone, lower basal cortisol ... "Elevated plasma corticotrophin-releasing hormone levels in veterans with posttraumatic stress disorder". Stress Hormones and ... Brain catecholamine levels are high,[88] and corticotropin-releasing factor (CRF) concentrations are high.[89][90] Together, ... "Corticotropin-releasing factor in posttraumatic stress disorder (PTSD) with secondary psychotic symptoms, nonpsychotic PTSD, ...
hormone activity. • corticotropin-releasing hormone receptor 1 binding. • corticotropin-releasing hormone receptor 2 binding. • ... Hormones (Athens). 2016. PMID 27377597.. *"Brain disorders associated with corticotropin-releasing hormone expression in the ... neuropeptide hormone activity. • receptor binding. • corticotropin-releasing hormone activity. Cydrannau o'r gell. • cytoplasm ... Protein sy'n cael ei godio yn y corff dynol gan y genyn CRH yw CRH a elwir hefyd yn Corticotropin releasing hormone (Saesneg). ...
... and also the effect of corticotropin-releasing hormone to stimulate secretion of ADH. ... Treatment involves replacing the absent hormones.[1] This involves taking a corticosteroid such as hydrocortisone and ... Addison's disease arises from problems with the adrenal gland such that not enough of the steroid hormone cortisol and possibly ... Hyponatremia (low blood sodium levels), due to loss of production of the hormone aldosterone, to the kidney's inability to ...
... of the pituitary gland in response to the hormone corticotropin-releasing hormone (CRH) released by the hypothalamus.[3] ACTH ... with a decrease in the release of corticotropin releasing hormone (CRH)). Conversely, chronically elevated ACTH levels occur in ... Adrenocorticotropic hormone (ACTH, also adrenocorticotropin, corticotropin) is a polypeptide tropic hormone produced by and ... This article is about adrenocorticotropic hormone as a natural hormone. For adrenocorticotropic hormone as a medication and ...
Corticotropin releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ...
MCs contain numerous granules and secrete an abundance of prestored mediators such as corticotropin-releasing hormone (CRH), ... Toxic materials produced or released[edit]. Examples of toxic materials produced or released by degranulation by granulocytes ... When an infection occurs, mature basophils will be released from the bone marrow and travel to the site of infection.[22] When ... Injured basophils and other leukocytes will release another substance called prostaglandins that contributes to an increased ...
Corticotropin-releasing hormone (1. *2). *EMR (1. *2. *3). *Glucagon (GR. *GIPR ... Also recently discovered A2B has Gq → DAG and IP3 → Release calcium → activate calmodulin → activate myosin light chain kinase ... Presynaptically, it reduces synaptic vesicle release while post synaptically it has been found to stabilize the magnesium on ... regulating the release of other neurotransmitters such as dopamine and glutamate,[6][7][8] while the A2B and A3 receptors are ...
Corticotropin releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... Cholecystokinin tetrapeptide (CCK-4, Trp-Met-Asp-Phe-NH2) is a peptide fragment derived from the larger peptide hormone ...
It comprises corticotropin-releasing factor (CRF), released by the hypothalamus; adrenocorticotropic hormone (ACTH), released ... The first of these factors to be identified are thyrotropin-releasing hormone (TRH) and gonadotropin-releasing hormone (GnRH). ... For example, the secretion of growth hormone is controlled by two neuroendocrine systems: the growth hormone-releasing hormone ... also called luteinizing hormone-releasing hormone) stimulates the secretion of luteinizing hormone and follicle-stimulating ...
... a corticotropin-releasing hormone receptor antagonist". Toxicology. 248 (1): 8-17. doi:10.1016/j.tox.2008.03.002. PMC 2424198. ...
"Corticotropin-Releasing Factor Receptors". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and ... Current status of the nomenclature for receptors for corticotropin-releasing factor and their ligands". Pharmacol. Rev. 55 (1 ... "Receptor-mediated actions of corticotropin-releasing factor in pituitary gland and nervous system". Neuroendocrinology 43 (1): ...
Corticotropin releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... "Press release: Merck Announces Second Quarter 2011 Financial Results". Merck. July 29, 2011. Archived from the original on ...
Corticotropin-releasing hormone (1. *2). *EMR (1. *2. *3). *Glucagon (GR. *GIPR ... 1.0 1.1 1.2 GRCh38: Ensembl release 89: ENSG00000050628 - Ensembl, May 2017 *↑ 2.0 2.1 2.2 GRCm38: Ensembl release 89: ... "Impaired adrenocorticotropic hormone response to bacterial endotoxin in mice deficient in prostaglandin E receptor EP1 and EP3 ...
Corticotropin releasing hormone. *Sauvagine. *Stressin I. *Urocortin. *Antagonists: Antalarmin. *Astressin-B. *CP-154,526 ... a b c GRCh38: Ensembl release 89: ENSG00000166573 - Ensembl, May 2017. *^ a b c GRCm38: Ensembl release 89: ENSMUSG00000024553 ... peptide hormone binding. • galanin receptor activity. • protein binding. Cellular component. • integral component of membrane. ...
... that the observed pulsatility of ACTH and glucocorticoids is driven via pulsatility of corticotropin-releasing hormone (CRH), ... Leutinizing Hormone & Follicle Stimulating Hormone[edit]. Main Article: Leutinizing Hormone LH is released from the pituitary ... gonadotropin-releasing hormone (GnRH) and growth hormone (GH). In the nervous system, pulatlility is observed in oscillatory ... "Intrinsic pulsatile secretory activity of immortalized luteinizing hormone-releasing hormone-secreting neurons". Proceedings of ...
... a nonpeptide corticotropin-releasing hormone (CRH) receptor antagonist: suppression of pituitary ACTH release and peripheral ... Potential uses of corticotropin-releasing hormone antagonists. Annals of the New York Academy of Sciences. 2006 Nov;1083:239-51 ... Antalarmin blockade of corticotropin releasing hormone-induced hypertension in rats. Brain Research. 2000 Oct 27;881(2):204-7. ... The impact of the nonpeptide corticotropin-releasing hormone antagonist antalarmin on behavioral and endocrine responses to ...
Corticotropin-releasing hormone receptor. References[edit]. *^ a b c GRCh38: Ensembl release 89: ENSG00000106113 - Ensembl, May ... peptide hormone binding. • corticotropin-releasing hormone receptor activity. Cellular component. • integral component of ... cellular response to corticotropin-releasing hormone stimulus. • G-protein coupled receptor signaling pathway. • hormone- ... "Entrez Gene: CRHR2 corticotropin releasing hormone receptor 2".. *^ Pal K, Swaminathan K, Xu HE, Pioszak AA (Dec 2010). " ...
Corticotropin-releasing hormone (CRH) (also known as corticotropin-releasing factor (CRF) or corticoliberin; corticotropin may ... Corticotropin-releasing hormone has been shown to interact with its receptors corticotropin-releasing hormone receptor 1 (CRFR1 ... corticotropin releasing hormone and corticotropin releasing hormone receptor genes are expressed in human skin". FEBS Lett. 374 ... It is a releasing hormone that belongs to corticotropin-releasing factor family. In humans, it is encoded by the CRH gene. Its ...
Corticotropin-releasing hormone receptors (CRHRs), also known as corticotropin-releasing factor receptors (CRFRs) are a G ... Corticotropin-releasing+hormone+receptors at the US National Library of Medicine Medical Subject Headings (MeSH) v t e v t e. ... This binding of corticotropin releasing-hormone (CRH) activates the hypothalamic-pituitary-adrenal (HPA) axis, one of the two ... "Corticotropin-Releasing Factor Receptors". IUPHAR Database of Receptors and Ion Channels. International Union of Basic and ...
This study sought to determine whether elevated levels of the brain peptide corticotropin releasing hormone (CRH), which ...
Immunoreactive corticotropin-releasing hormone and its binding sites in the rat ovary.. G Mastorakos, E L Webster, T C Friedman ... Corticotropin-releasing hormone (CRH), the principal neuropeptide regulator of pituitary ACTH secretion, is also produced at ...
Is 11β-HSD1 expressed in islet β-cells and regulated by corticotropin-releasing hormone?. Jun-Li Liu, Coimbatore B. Srikant, ... 6C showing corticotropin-releasing hormone-induced inhibition also becomes questionable.. Acknowledgments. Research funded by ... Is 11β-HSD1 expressed in islet β-cells and regulated by corticotropin-releasing hormone? ... Is 11β-HSD1 expressed in islet β-cells and regulated by corticotropin-releasing hormone? ...
This invention provides members of the corticiotropin-releasing hormone superfamily and peptide analogs thereof wherein the 38, ... Slominski et al., "Proopiomelanocortin, corticotropin releasing hormone and corticotropin releasing hormone receptor genes are ... Corticotropin-releasing hormone analogs. 2005-02-01. Wei et al.. 6319900. Inhibition of abnormal cell growth with corticotropin ... Corticotropin releasing hormone and the skin. Frontiers in Biosci. 11: 2230-2248, Sep. 1, 2006. Beyermann et al. A Single-Point ...
Corticotropin-releasing hormone induces Fas ligand production and apoptosis in PC12 cells via activation of p38 mitogen- ... Corticotropin releasing hormone neurons in the paraventricular nucleus are direct targets for neuropeptide Y neurons in the ... Hypotensive hemorrhage elevates corticotropin-releasing hormone messenger ribonucleic acid (mRNA) but not vasopressin mRNA in ... Increased expression of corticotropin-releasing hormone and vasopressin messenger ribonucleic acid (mRNA) in the hypothalamic ...
Transcription of the human corticotropin-releasing hormone gene in NPLC cells is correlated with Z-DNA formation. S Wölfl, C ... The intron of the corticotropin-releasing hormone (corticoliberin; CRH) gene contains a sequence of over 100 bp of alternating ... Transcription of the human corticotropin-releasing hormone gene in NPLC cells is correlated with Z-DNA formation ... Transcription of the human corticotropin-releasing hormone gene in NPLC cells is correlated with Z-DNA formation ...
Receptors, Corticotropin-Releasing Hormone*Receptors, Corticotropin-Releasing Hormone. *Corticotropin-Releasing Hormone ... Receptors, Pituitary Hormone-Regulating Hormone [D12.776.543.750.750.700]. *Receptors, Corticotropin-Releasing Hormone [D12.776 ... The corticotropin releasing-hormone receptors on anterior pituitary cells mediate the stimulation of corticotropin release by ... hypothalamic corticotropin releasing factor. The physiological consequence of activating corticotropin-releasing hormone ...
Corticotropin-releasing hormone drives anandamide hydrolysis in the amygdala to promote anxiety.. [J Megan Gray, Haley A ... Corticotropin-releasing hormone (CRH) is a central integrator in the brain of endocrine and behavioral stress responses, ...
Corticotropin-releasing hormone takes the heat off sex reversal Message Subject (Your Name) has sent you a message from ... They show that corticotropin-releasing hormone B (crhb) is upregulated in embryos incubated at high temperature during the ...
Brain disorders associated with corticotropin-releasing hormone expression in the placenta among children born before the 28th ... To evaluate the relationship between placenta corticotropin-releasing hormone (CRH) expression and brain structure and function ...
Mechanisms of action of corticotropin-releasing factor and other regulators of corticotropin release in rat pituitary cells. J ... Luo X, Kiss A, Makara G, Lolait SJ, Aguilera G (1994) Stress-specific regulation of corticotropin releasing hormone receptor ... Ma XM, Aguilera G (1999a) Transcriptional responses of the vasopressin and corticotropin-releasing hormone genes to acute and ... Ma XM, Camacho C, Aguilera G (2001) Regulation of corticotropin-releasing hormone (CRH) transcription and CRH mRNA stability by ...
Corticotropin-releasing hormone and postpartum depression: A longitudinal study. Iliadis, Stavros Uppsala University, ...
neuropeptide Y, corticotropin-releasing hormone, anxiety, stress National Category Neurosciences Identifiers. URN: urn:nbn:se: ... Brain neuropeptide Y and corticotropin-releasing hormone in mediating stress and anxiety. Thorsell, Annika National Institute ... Neuropeptides such as neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) have been implicated not only in acute ...
Skin expression levels of the POMC gene and POMC/corticotropin releasing hormone (CRH) peptides ar … ... derived neuropeptides alpha-melanocyte stimulating hormone (alpha-MSH), beta-endorphin, and ACTH and also a source of these ... Corticotropin releasing hormone and proopiomelanocortin involvement in the cutaneous response to stress Physiol Rev. 2000 Jul; ... Skin expression levels of the POMC gene and POMC/corticotropin releasing hormone (CRH) peptides are not static but are ...
Corticotropin-Releasing Hormone. Epinephrine. Racepinephrine. Epinephryl borate. Hormones, Hormone Substitutes, and Hormone ... Corticotropin Releasing Hormone (CRH) is a hypothalamic hormone made up of 41 amino acids. Amino acids are proteins that when ... Corticotropin-releasing hormone (CRH) is a 41 amino acid hypothalamic peptide whose chemical structure has recently been ... Dose Response Relationship for Single Doses of Corticotropin Releasing Hormone (CRH) in Normal Volunteers and in Patients With ...
Effect of acute ether or restraint stress on plasma corticotropin-releasing hormone, vasopressin and oxytocin levels in the rat ... Ether and restraint stress-induced peripheral plasma corticotropin releasing hormone (CRH), arginine vasopressin (AVP), ... The levels of stress-induced CRH in the peripheral plasma were sufficient to stimulate ACTH release. These results suggest that ...
Increased expression of corticotropin-releasing hormone and vasopressin messenger ribonucleic acid (mRNA) in the hypothalamic ... in corticosteroid receptor function could potentially contribute to the putative shift from corticotropin-releasing hormone ( ...
The class B corticotropin-releasing hormone type 1 receptor (CRHR1) is a key player in the stress response whose dysregulation ... A fluorescence nanoscopy marker for corticotropin-releasing hormone type 1 receptor: computer design, synthesis, signaling ... A fluorescence nanoscopy marker for corticotropin-releasing hormone type 1 receptor: computer design, synthesis, signaling ...
Corticotropin-releasing hormone (CRH) was infused intracerebroventricularly into rats for 7 d via a miniosmotic pump (1 μg · μl ... 1990) Preoptic area injection of corticotropin-releasing hormone stimulates sympathetic activity. Am J Physiol 259:R799-R806. ... 1995) Corticotropin-releasing hormone mRNA levels in the paraventricular nucleus of patients with Alzheimers disease and ... Corticotropin-releasing hormone (CRH) is widely distributed throughout the brain and acts as a putative neurotransmitter/ ...
Corticotropin Releasing Hormone (CRH) system and inflammation. Katia Karalis1, Christina Chandras1 & Thalia Teli1. ... Corticotropin Releasing Hormone (CRH) is the hypothalamic mediator of the stress response that ultimately results in increased ... release of glucocorticoid. CRH exerts its effects by binding to the CRH receptors 1 and 2 that belong to the family of the ...
Corticotropin-releasing hormone. Corticotropin-Releasing Factor and Interleukin-1? are Involved in the Electroacupuncture ... Corticotropin-Releasing Factor and Interleukin-1? are Involved in the Electroacupuncture-Induced Analgesic Effect on ...
... was studied in 12 amenorrheic and in 9 eumenorrheic athletes by comparing the concentrations of corticotropin-releasing hormone ... CRH), corticotropin (ACTH), and endorphins (beta-endorphin + beta-lipotro ... Adrenocorticotropic Hormone / blood*. Amenorrhea / blood*, etiology. Corticotropin-Releasing Hormone / blood*. Endorphins / ... Plasma corticotropin-releasing hormone, corticotropin, and endorphins at rest and during exercise in eumenorrheic and ...
Advances in the development of corticotropin-releasing-hormone (CRH) receptor agonists as candidate analgesics : Pharmaceutical ... One target for the development of analgesics is corticotropin-releasing-hormone (CRH). This peptide is released by the ... A recent study has demonstrated the analgesic activity of corticotropin-releasing-hormone (CRH) and has shown that this ... Advances in the development of corticotropin-releasing-hormone (CRH) receptor agonists as candidate analgesics. Posted on: 21 ...
Corticotropin-releasing hormone (CRH) load test: after intravenous injection of CRH (0.1 mg), ACTH and cortisol levels were ... We conducted several hormone load tests. In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ... We conducted several hormone load tests. In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ... Second, we conducted several hormone load tests (Figure 1). In corticotropin-releasing hormone (CRH) load test, excess and ...
Stress stimulates the hypothalamic-pituitary-adrenal axis through the release of corticotropin-releasing hormone (CRH),4 which ... Pleiotropic effects of corticotropin releasing hormone on normal human skin keratinocytes. In Vitro Cell. Dev. Biol. Anim. 37: ... Corticotropin-releasing hormone mimics stress-induced colonic epithelial pathophysiology in the rat. Am. J. Physiol. 277: G391- ... Characterization of corticotropin-releasing hormone binding sites in the human placenta. J. Recept. Signal Transduct. Res. 17: ...
RelB/p52-mediated NF-κB signaling alters histone acetylation to increase the abundance of corticotropin-releasing hormone in ... RelB/p52-mediated NF-κB signaling alters histone acetylation to increase the abundance of corticotropin-releasing hormone in ... RelB/p52-mediated NF-κB signaling alters histone acetylation to increase the abundance of corticotropin-releasing hormone in ... RelB/p52-mediated NF-κB signaling alters histone acetylation to increase the abundance of corticotropin-releasing hormone in ...
Corticotropin-releasing Hormone and Endocannabinoids. In: Kordon C., Gaillard RC., Christen Y. (eds) Hormones and the Brain. ... Corticotropin-releasing hormone-mediated neuroprotection against oxidative stress is associated with the increased release of ... the corticotropin-releasing hormone (CRH) and endogenously produced and secreted cannabinoids (endocannabinoids). These ... Brain region-specific neuroprotective action and signaling of corticotropin-releasing hormone in primary neurons. Endocrinoloy ...
  • The portal system carries the CRH to the anterior lobe of the pituitary, where it stimulates corticotropes to secrete adrenocorticotropic hormone (ACTH) and other biologically-active substances (β-endorphin). (
  • Cells in the anterior lobe of the pituitary gland known as corticotropes express the receptors and will secrete adrenocorticotropic hormone (ACTH) when stimulated. (
  • Expression of proopiomelanocortin (POMC)-derived melanocyte-stimulating hormone (MSH) and adrenocorticotropic hormone (ACTH) peptides in skin of basal cell carcinoma patients" Hum. (
  • This peptide is released by the hypothalamus and stimulates the anterior pituitary cortex to release adrenocorticotropic hormone, which then activates the adrenal gland to release corticosteroids. (
  • In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ACTH (adrenocorticotropic hormone) was observed, indicating the dysfunction of the hypothalamus. (
  • Stress initiates hypothalamic release of corticotropin-releasing hormone (CRH), which stimulates secretion of adrenocorticotropic hormone from the pituitary and thereby increased glucocorticoid production by the adrenal cortex. (
  • Methods -CRH (2 μg/kg) was intravenously administered during duodenal and colonic manometry and plasma adrenocorticotropic hormone (ACTH) was measured by radioimmunoassay. (
  • There, CRH causes the anterior pituitary gland to release adrenocorticotropic hormone (ACTH). (
  • After the hypothalamus (the part of the brain containing secretions important to metabolic activities) sends "releasing hormones" to the pituitary gland , the pituitary secretes a hormone called adrenocorticotropic hormone (ACTH). (
  • adrenocorticotropic hormone (ACTH) corticotropin . (
  • First, an injection of urocortin-2 (7.5 µg) into the lateral ventricle resulted in transient increases in CRH heteronuclear RNA (hnRNA) in parvocellular paraventricular nucleus (PVN) and in plasma adrenocorticotropic hormone (ACTH), whereas sustained increases in arginine vasopressin (AVP) hnRNA and c-fos mRNA in the parvocellular PVN were observed as compared with vehicle treatment. (
  • Low plasma cortisol results in increased production of adrenocorticotropic hormone (ACTH) from the anterior pituitary gland, due to the lack of feedback inhibition. (
  • This paper highlights the problem of neuroendocrine tumours (NETs) with clinical symptoms of hypercorticism caused by hypersecretion of adrenocorticotropic hormone (ACTH) by tumour cells. (
  • Corticotropin-releasing hormone (CRH), the principal neuropeptide regulator of pituitary ACTH secretion, is also produced at peripheral inflammatory sites, where it acts as a proinflammatory cytokine, and by the Leydig cell of the testis, where it exerts autocrine inhibition of testosterone biosynthesis. (
  • The skin is a known target organ for the proopiomelanocortin (POMC)-derived neuropeptides alpha-melanocyte stimulating hormone (alpha-MSH), beta-endorphin, and ACTH and also a source of these peptides. (
  • When CRH is released from the hypothalamus it stimulates the pituitary gland to secrete another hormone, ACTH. (
  • ACTH then causes the adrenal glands to make a third hormone, cortisol. (
  • Ether and restraint stress-induced peripheral plasma corticotropin releasing hormone (CRH), arginine vasopressin (AVP), oxytocin (OXY) and adrenocorticotropin (ACTH) levels were measured by radioimmunoassays. (
  • The levels of stress-induced CRH in the peripheral plasma were sufficient to stimulate ACTH release. (
  • The hypothalamic-pituitary response to exercise was studied in 12 amenorrheic and in 9 eumenorrheic athletes by comparing the concentrations of corticotropin-releasing hormone (CRH), corticotropin (ACTH), and endorphins (beta-endorphin + beta-lipotropin) in plasma at rest and during an acute exercise on a bicycle ergometer requiring 80% and 100% of the maximal oxygen uptake (VO2 max). (
  • In corticotropin-releasing hormone (CRH) load test, excess and delayed reaction of ACTH was observed. (
  • Corticotropin-releasing hormone (CRH) load test: after intravenous injection of CRH (0.1 mg), ACTH and cortisol levels were examined. (
  • Release of the peptides corticotropin-releasing hormone (CRH) and vasopressin (VP) from PVN parvocellular neurons in the hypophyseal portal blood stimulates the release of ACTH ( 46 , 55 ) from the anterior pituitary, which subsequently stimulates the production and release of glucocorticoids from the adrenal cortex. (
  • Magnocellular-derived VP has been implicated in facilitating release of ACTH in response to stress ( 17 ). (
  • The Corticotropin-Releasing Hormone Stimulation Blood Test consists of measuring ACTH and cortisol levels, then administering CRH and measuring ACTH and cortisol levels 5, 10, 15, 30, 45, 60, 90, and 120 minutes after CRH administration. (
  • Cortisol is another stress hormone produced by the adrenal glands in response to ACTH. (
  • After ACTH causes the adrenal gland to release its various hormones, these hormones act back on the hypothalamus and pituitary glands to prevent further release of hormones. (
  • The Corticotropin-Releasing Hormone Stimulation Blood Test assesses the negative feedback process of CRH and ACTH. (
  • The ACTH then travels through the bloodstream to the adrenal cortex, where it encourages the production and release of cortisol (sometimes called the "stress" hormone) and other adrenocortical hormones. (
  • Adrenocorticotropin hormone, or ACTH, is a hormone made by the pituitary gland that stimulates the adrenal glands to make cortisol. (
  • Then, corticotropin-releasing hormone -- a chemical that stimulates the release of ACTH -- is injected. (
  • Typically, ACTH levels peak after 15 to 30 minutes, and cortisol levels peak 30 to 40 minutes after the injection of corticotropin-releasing hormone. (
  • Reimondo G, Paccotti P, Minetto M, Termine A, Stura G, Bergui M. The corticotrophin-releasing hormone test is the most reliable noninvasive method to differentiate pituitary from ectopic ACTH secretion in Cushing's syndrome. (
  • To the Editor: The report by Gold and colleagues (May 22 issue) 1 indicated that the plasma ACTH response to ovine corticotropin-releasing hormone stimulation can be helpful in the differential diagnosis of two conditions of hypercortisolism - the depressive phase of primary affective disorder and Cushing's disease. (
  • CRH is known as the main stimulator of ACTH release. (
  • The precursor to ACTH, pro-opiomelanocortin (POMC), also contains melanocyte-stimulating hormone (MSH), which is released with the production of ACTH. (
  • Preoperative imaging identification and localization of adrenocorticotropin hormone (ACTH)-secreting pituitary adenomas is critical for the accurate diagnosis and the successful surgical treatment of Cushing s disease (CD). (
  • Moreover, corticotropin-releasing hormone (CRH) can be given to selectively increase the metabolic activity of ACTH-secreting pituitary adenomas to increase the likelihood of their detection and localization by (18)F-FDG PET-imaging. (
  • CRF 2 receptors are type 2 G protein-coupled receptors for corticotropin-releasing hormone (CRH) that are resident in the plasma membranes of hormone-sensitive cells. (
  • The N-terminal signal peptides of corticotropin-releasing hormone receptor 1 and CRHR2 beta are cleaved off in the endoplasmic reticulum to yield the mature receptors. (
  • Corticotropin-releasing hormone has been shown to interact with its receptors corticotropin-releasing hormone receptor 1 (CRFR1) and corticotropin-releasing hormone 2 (CRFR2) in order to induce its effects. (
  • Corticotropin-releasing hormone receptors (CRHRs), also known as corticotropin-releasing factor receptors (CRFRs) are a G protein-coupled receptor family that binds corticotropin-releasing hormone (CRH). (
  • Receptors, Corticotropin-Releasing Hormone" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (
  • The corticotropin releasing-hormone receptors on anterior pituitary cells mediate the stimulation of corticotropin release by hypothalamic corticotropin releasing factor. (
  • The physiological consequence of activating corticotropin-releasing hormone receptors on central neurons is not well understood. (
  • This graph shows the total number of publications written about "Receptors, Corticotropin-Releasing Hormone" by people in Harvard Catalyst Profiles by year, and whether "Receptors, Corticotropin-Releasing Hormone" was a major or minor topic of these publication. (
  • Below are the most recent publications written about "Receptors, Corticotropin-Releasing Hormone" by people in Profiles. (
  • 1996) Neurobiology of corticotropin releasing factor (CRF) receptors and CRF-binding protein: implications for the treatment of CNS disorders. (
  • Corticotropin releasing factor receptors and their ligand family. (
  • Corticotropin is the main hormone secreted from pituitary gland responding to stress and has two receptors to bind the target tissues such as uterus and gut, named CRHR1 and CRHR2. (
  • corticotropin-releasing hormone (CRH) a neuropeptide secreted by the median eminence of the hypothalamus that binds to specific receptors on the corticotroph cells of the anterior pituitary and stimulates the secretion of corticotropin . (
  • Lastly, the mRNA levels of hormones and receptors involved in the control of thyroidal and adrenal function were measured by qPCR in zebra finch chicks between hatching and fledging, and in adults. (
  • We have investigated which cell types and receptors are involved in CRH-induced TSH release in the chicken (Gallus gallus). (
  • In this review, we focus on the regulation of gonadotropins by CRF and Ucn2 in pituitary gonadotrophs and of gonadotropin-releasing hormone (GnRH) via CRF receptors in the hypothalamus. (
  • corticotropin may also be spelled corticotrophin) is a peptide hormone involved in the stress response. (
  • Corticotropin-releasing hormone (CRH) is a 41-amino acid peptide derived from a 196-amino acid preprohormone. (
  • This study sought to determine whether elevated levels of the brain peptide corticotropin releasing hormone (CRH), which inhibits feeding in fibrosarcoma tumor-bearing rats, promotes anorexia. (
  • This invention provides members of the corticiotropin-releasing hormone superfamily and peptide analogs thereof wherein the 38thamino acid from the N-terminus is D-Nle, i.e. (
  • Corticotropin-releasing hormone (CRH) is a 41 amino acid hypothalamic peptide whose chemical structure has recently been determined after more than two decades of intensive research. (
  • Human stresscopin and stresscopin-related peptide are selective ligands for the type 2 corticotropin-releasing hormone receptor. (
  • Endocrine and cardiovascular responses to corticotropin-releasing hormone in patients with posttraumatic stress disorder: A role for atrial natriuretic peptide? (
  • Corticotropin-releasing factor (CRF), a peptide first isolated from mammalian brain, is critical in the regulation of the pituitary-adrenal axis, and in complementary stress-related endocrine, autonomic and behavioural responses. (
  • Synthetic peptide against 19 amino acids from the N-terminal extracellular domain of the Human Corticotropin Releasing Factor Receptor 2 protein (Q13324). (
  • Corticotropin-releasing factor (CRF) is a major regulatory peptide in the HPA axis during stress. (
  • CRH: This hormone from hypothalamus regulates the release of corticotropin from pituitary gland. (
  • Regulation of hormone production and release from the adrenal cortex involves the pituitary gland , a small gland located at the base of the brain. (
  • In chicken, corticotropin-releasing hormone (CRH) acts as a thyrotropin (TSH)-releasing factor, mediated by the type 2 CRH receptor (CRHR2) on the thyrotropes of the pituitary gland. (
  • Stress stimulates the hypothalamic-pituitary-adrenal axis through the release of corticotropin-releasing hormone (CRH), 4 which activates behavioral, autonomic and endocrine responses, leading to secretion of glucocorticoids that down-regulate immune responses ( 4 ). (
  • Whereas dehydration stimulates VP release in the systemic circulation ( 18 ), drinking after a period of water deprivation causes a rapid decrease in plasma VP ( 4 , 19 , 49 , 52 ). (
  • which, in turn, stimulates the release of glucocorticoids from the adrenal glands ( Whitnall, 1993 ). (
  • CRH is produced by parvocellular neuroendocrine cells within the paraventricular nucleus of the hypothalamus and is released at the median eminence from neurosecretory terminals of these neurons into the primary capillary plexus of the hypothalamo-hypophyseal portal system. (
  • Chronic CRH depletion from GABAergic, long-range projection neurons in the extended amygdala reduces dopamine release and increases anxiety. (
  • Bayatti N, Zschocke J, Behl C (2003) Brain region-specific neuroprotective action and signaling of corticotropin-releasing hormone in primary neurons. (
  • The present study monitored Fos-like immunoreactivity (Fos) to assess the effect of WR-induced drinking on the activity of vasopressin (VP)-positive magnocellular and parvocellular neurons and corticotropin-releasing hormone (CRH)-positive parvocellular neurons in the paraventricular nucleus of the hypothalamus. (
  • Dendritic cell nuclear protein-1 was also found to be co-localized with corticotropin-releasing hormone in paraventricular nucleus neurons. (
  • Corticotropin-releasing hormone neurons in the paraventricular nucleus of the hypothalamus reside at the apex of this stress signaling axis, so any genetic or environmental insult to the normal modulation of their activity can profoundly disrupt healthy stress signaling. (
  • tionally, there exist corticotropin-releasing hormone neurons in other brain regions, notably the hippocampus. (
  • and second, to explore the characteristics and functional relevance of hippocampal corticotropin-releasing hormone neurons, with particular emphasis on their stress-reactivity and impact on the excitability of the hippocampal network. (
  • I confirmed that inhibitory constraint of hypothalamic corticotropin-releasing hormone neurons is critical for regulating stress-reactive emotional behaviors, and helped to reveal that this inhibitory constraint is compromised following seizures. (
  • In the course of my hippocampus-oriented project, I characterized back-projecting corticotropin-releasing hormone neurons as a novel interneuron population. (
  • Phumsatitpong, Chayarndorn;Moenter, Suzanne M 2018-01-01 00:00:00 Abstract Gonadotropin-releasing hormone (GnRH) neurons are the final central regulators of reproduction, integrating various inputs that modulate fertility. (
  • Gonadotropin-releasing hormone (GnRH) neurons are crucial regulators of the reproductive system. (
  • Rapid phosphorylation of the CRE binding protein precedes stress-induced activation of the corticotropin releasing hormone gene in medial parvocellular hypothalamic neurons of the immature rat. (
  • The neuroendocrine stress response is controlled by corticotropin-releasing hormone (CRH) neurons located within the paraventricular nucleus (PVN) of the hypothalamus. (
  • During stress, noradrenaline (NA) is released within the PVN to activate CRH neurons and drive stress hormone secretion. (
  • Lastly, we showed that release of intracellular calcium does not appear to play an important role in NA-induced calcium elevations in CRH neurons, and blockade of intracellular calcium re-uptake with CPA (30 µM) (n = 9 slices) appears to enhance CRH neuron excitation. (
  • Lhx6-positive GABA-releasing neurons of the zona incerta promote sleep. (
  • The neuroendocrine stress response is initiated by excitation of corticotropin-releasing hormone (CRH) neurons in the paraventricular nucleus of the hypothalamus. (
  • Repetitive excitatory input to neurons causes the release of endocannabinoids (eCBs). (
  • As oxytocin has been shown to stimulate the release of eCBs from neurons, we investigated whether oxytocin was able to inhibit currents onto CRH neurons. (
  • We also show, for the first time, that depolarisation- induced release of eCBs is able to activate the TRPV1 channel to increase spontaneous currents onto CRH neurons. (
  • Corticotropin-releasing hormone ( CRH ), originally named corticotropin-releasing factor ( CRF ), and also called corticoliberin , is a polypeptide hormone and neurotransmitter involved in the stress response. (
  • Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explaination for its proinflammatory effects," Endocrinology, vol. 139, 1998, pp. 403-413. (
  • D-Amino Acid-Substituted Analogs of Corticotropin-Releasing Hormone (CRH) and Urocortin with Selective Agonist Activity at CRH.sub.1 and CRH.sub.2.beta. (
  • Identification of urocortin III, an additional member of the corticotropin-releasing factor (CRF) family with high affinity for the CRF2 receptor. (
  • G-protein coupled receptor for CRH (corticotropin-releasing factor), UCN (urocortin), UCN2 and UCN3. (
  • Urocortin, a mammalian neuropeptide related to fish urotensin I and to corticotropin-releasing factor. (
  • The involvement of this CRH receptor in the response of thyrotropes to CRH was further confirmed by the fact that TSH release was stimulated by human urocortin III, a CRH-R2-specific agonist, whereas the TSH response to CRH was completely blocked by the CRH-R blocker astressin and the CRH-R2-specific antagonist antisauvagine-30. (
  • Nieman LK, Oldfield EH, Wesley R, Chrousos GP, Loriaux DL, Cutler GB Jr. A simplified morning ovine corticotropin-releasing hormone stimulation test for the differential diagnosis of adrenocorticotropin-dependent Cushing's syndrome. (
  • The role of glucocorticoids and the repressor isoform of cAMP response element (CRE) modulator (CREM), inducible cAMP early repressor (ICER), in limiting corticotropin-releasing hormone (CRH) transcription during restraint stress were examined in both intact and adrenalectomized rats receiving glucocorticoid replacement. (
  • Corticotropin Releasing Hormone (CRH) is the hypothalamic mediator of the stress response that ultimately results in increased release of glucocorticoid. (
  • An N-ethyl-N-nitrosourea induced Corticotropin releasing hormone promoter mutation provides a mouse model for endogenous glucocorticoid excess. (
  • Cortisol, a very potent glucocorticoid - a group of adrenocortical hormones that protects the body from stress and affect protein and carbohydrate metabolism - is involved in regulating the functioning of nearly every type of organ and tissue in the body, and is considered to be one of the few hormones absolutely necessary for life. (
  • The most common cause of Cushing's syndrome is the long-term use of glucocorticoid hormones in medications. (
  • such 'anticipatory' signals regulate glucocorticoid release under conditions in which physical challenges may be predicted, either by innate programs or conditioned stimuli. (
  • The release of cytokines, such as tumor necrosis factor-α, is thought to compete with corticotropin releasing hormone (CRH) for glucocorticoid regulation and may also induce tissue resistance to glucocorticoids. (
  • abstract = "Corticotropin-releasing hormone (CRH) is a hypothalamic neuropeptide that has been identified also in several peripheral tissues, including organs of the reproductive system. (
  • abstract = "The actions of corticotropin-releasing hormone (CRH) on steroidogenesis in enriched preparations of mouse and rat Leydig cells were investigated. (
  • Neuropeptides such as neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH) have been implicated not only in acute regulation of stress/anxiety-related behaviors, but adaptations and changes in these neuropeptide systems may also participate in the regulation of behavior and endocrine responses during chronic stress. (
  • Placental corticotropin-releasing hormone: function and regulation. (
  • The activation of type 1 corticotropin releasing factor receptor (CRF-R1) inhibits proliferation and promotes differentiation of neuroblastoma cells in vitro via p27(Kip1) protein up-regulation and c-Myc mRNA down-regulation. (
  • 2004). "Paracrine regulation of endometrial function: interaction between progesterone and corticotropin-releasing factor (CRF) and activin A.". Steroids 68 (10-13): 801-7. (
  • 5 6 These phenomena in rats are mimicked by intracerebroventricular 6-9 or intravenous 9 administration of corticotropin releasing hormone (CRH) and are blocked by the CRH antagonist, α helical CRH 9-41 . (
  • The administration of corticotropin‐releasing hormone produced age‐specific seizures within minutes, which correlated with rhythmic amygdala discharges. (
  • Human Corticotropin-Releasing Hormone tests: 10 years of real-life experience in pituitary and adrenal disease. (
  • 1990). "Structural analysis of the regulatory region of the human corticotropin releasing hormone gene. (
  • Should the Human Corticotropin Releasing Hormone Binding Protein (CRHBP) ELISA Kit is proven to show malperformance, you will receive a refund or a free replacement. (
  • Description: A sandwich quantitative ELISA assay kit for detection of Human Corticotropin Releasing Hormone Binding Protein (CRHBP) in samples from serum, plasma or other biological fluids. (
  • Description: This is Double-antibody Sandwich Enzyme-linked immunosorbent assay for detection of Human Corticotropin Releasing Hormone Binding Protein (CRHBP) in serum, plasma and other biological fluids. (
  • We propose that full-length dendritic cell nucleus protein-1 may play a role in the pathogenesis of depressive disorders by enhancing corticotropin-releasing hormone expression in the hypothalamic paraventricular nucleus. (
  • Corticotropin-releasing hormone is secreted by the paraventricular nucleus (PVN) of the hypothalamus in response to stress. (
  • Corticotropin-releasing hormone receptor 2 ( CRHR2 ) is a protein , also known by the IUPHAR -recommended name CRF 2 , [5] that is encoded by the CRHR2 gene and occurs on the surfaces of some mammalian cells. (
  • Lezoualc'h F, Engert S, Berning B, Behl C (2000) Corticotropin-releasing hormone-mediated neuroprotection against oxidative stress is associated with the increased release of non-amyloidogenic amyloid beta precursor protein and with the suppression of nuclear factor-kappaB. (
  • In the present study we investigate whether the two forms of dendritic cell nuclear protein-1 might act on corticotropin-releasing hormone, which plays a crucial role in the stress response and in the pathogenesis of depression. (
  • Moreover, full-length dendritic cell nucleus protein-1 bound to and transactivated the promoter of corticotropin-releasing hormone in human embryonic kidney 293 cells. (
  • Marked reduction in this protein has been observed in association with Alzheimer disease and autosomal recessive hypothalamic corticotropin deficiency has multiple and potentially fatal metabolic consequences including hypoglycemia and hepatitis. (
  • A rapid increase in circulating levels of the hormone occurs at the onset of parturition, suggesting that, in addition to its metabolic functions, this protein may act as a trigger for parturition. (
  • The protein encoded by this gene belongs to the G-protein coupled receptor 2 family, and the subfamily of corticotropin releasing hormone receptor. (
  • Here you will find information and further literature on rhCG - Corticotropin releasing hormone binding protein. (
  • In islets cultured under normoxia, CRH stimulated insulin release in a glucose- and CRH-level-dependent manner by activating CRHR1 and thus the cAMP-dependent protein kinase pathway and calcium influx through L-type channels. (
  • Antidepressant Outcomes Predicted by Genetic Variation in Corticotropin-Releasing Hormone Binding Protein. (
  • The authors found that the rs28365143 variant within the corticotropin-releasing hormone binding protein (CRHBP) gene predicted antidepressant outcomes for remission, response, and symptom change. (
  • No Association Between Antidepressant Efficacy and rs28365143 in Corticotropin-Releasing Hormone Binding Protein in a Large Meta-Analysis. (
  • One of the best-known endocrine hormones is insulin , a protein manufactured by the beta cells of the islands of Langerhans in the pancreas that is important in carbohydrate metabolism. (
  • This is a receptor for corticotropin releasing factor. (
  • Skin expression levels of the POMC gene and POMC/corticotropin releasing hormone (CRH) peptides are not static but are determined by such factors as the physiological changes associated with hair cycle (highest in anagen phase), ultraviolet radiation (UVR) exposure, immune cytokine release, or the presence of cutaneous pathology. (
  • Glucocorticoids epigenetically induce the expression of a stress hormone gene associated with labor in human placenta cells. (
  • The relatively recent advent of genetic tools to isolate specific cell types in the brain for identification and manipulation provided the foundation for my investigations of these two neuronal populations: specifically, a transgenic mouse line that expresses Cre recombinase under the control of the promoter for the corticotropin-releasing hormone gene. (
  • Corticotropin-releasing hormone links pituitary adrenocorticotropin gene expression and release during adrenal insufficiency. (
  • Entrez Gene: CRH corticotropin releasing hormone. (
  • Rapid sequential intravenous administration of four hypothalamic releasing hormones as a combined anterior pituitary function test in normal subjects. (
  • The class B corticotropin-releasing hormone type 1 receptor (CRHR1) is a key player in the stress response whose dysregulation is critically involved in stress-related disorders: psychiatric conditions ( i.e. depression, anxiety, and addictions), neuroendocrinological alterations, and neurodegenerative diseases. (
  • In luteinizing hormone-releasing hormone (LHRH) load test, delayed reaction of LH and FSH (follicle stimulating hormone) was observed, which was also compatible with the possible dysfunction of the hypothalamus. (
  • Corticotropin-releasing hormone (CRH) is a hormone that is produced by the hypothalamus of the brain. (
  • Corticotropin-releasing hormone (CRH) is a central integrator in the brain of endocrine and behavioral stress responses, whereas activation of the endocannabinoid CB1 receptor suppresses these responses. (
  • In particular this invention relates to the polypeptides as well as to the polynucleotides encoding these polypeptides, wherein said polypeptides are shown to play a central role in mediating the endocrine response to corticotropin releasing hormone. (
  • Cushing's syndrome is a relatively rare endocrine (hormonal) disorder resulting from excessive exposure to the hormone cortisol. (
  • Hormones are produced by various organs and body tissues, but mainly by the endocrine glands , such as the pituitary, thyroid, and gonads (testes and ovaries). (
  • Animal hormones can also be used, as endocrine hormones are to some extent interchangeable among species. (
  • Endocrine hormone synthesis and secretion is controlled and regulated by a closed-loop system. (
  • It is not known exactly how the synthesis and secretion of endocrine hormones from nonendocrine tissues occurs. (
  • Diurnal variation in the response of plasma adrenocorticotropin and cortisol to intravenous ovine corticotropin-releasing hormone. (
  • GnRH pulses stimulate secretion of the gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone, which then induce the gonads to activate gametogenesis and steroidogenesis. (
  • This binding of corticotropin releasing-hormone (CRH) activates the hypothalamic-pituitary-adrenal (HPA) axis, one of the two parts of the fight-or-flight response to stress. (
  • entitled "Modulation of pancreatic islets-stress axis by hypothalamic releasing hormones and 11β-hydroxysteroid dehydrogenase" (11β-HSD) ( 1 ). (
  • Effect of acute ether or restraint stress on plasma corticotropin-releasing hormone, vasopressin and oxytocin levels in the rat. (
  • CRH plays a pivotal effect in the stress response of an organi sm and it also has the potential to modulate pain tran sm ission in part by its effect on the release of beta-endorphin from the pituitary. (
  • Corticotropin-releasing hormone (CRH), which activates the hypothalamic-pituitary-adrenal axis under stress, also has proinflammatory peripheral effects possibly through mast cells. (
  • It was previously shown that acute psychological stress by immobilization results in dura mast cell degranulation, an effect blocked by pretreatment with antiserum against corticotropin-releasing hormone (CRH). (
  • The effect of psychological stress was investigated on rat cardiac mast cells, because their release of coronary constrictive and proinflammatory molecules contributes to myocardial ischemia and possibly arrhythmias. (
  • These results indicate acute stress could result in local CRH and nonpeptide neurotensin release which could contribute to myocardial pathophysiology through direct or indirect release of cardiac mast cell mediators. (
  • We report that acute psychological stress causes cardiac mast cell degranulation through local release of CRH and NT. (
  • Corticotropin-releasing hormone (CRH) released during the stress response may suppress reproduction independent of downstream glucocorticoids. (
  • A principal regulator of the these responses in both mature and developing rat is the neuropeptide corticotropin releasing hormone (CRH), and levels of hypothalamic CRH mRNA are enhanced by stress. (
  • Corticotropin-releasing hormone mimics stress-induced colonic epithelial pathophysiology in the rat. (
  • 2003). "Placental stress factors and maternal-fetal adaptive response: the corticotropin-releasing factor family. (
  • It eventually causes the release of stress hormones such as cortisol and aldosterone. (
  • In addition to stress hormones, the adrenal glands also produce hormones that regulate electrolyte levels. (
  • Despite the well-documented role of corticotropin-releasing hormone receptor (CHRH) in stress-related disorders, reproductive function, and inflammation , this is the first experimental study that addressed the role of CHRH1 blocage in the treatment of endometriosis. (
  • Corticotropin-releasing hormone (CRH) helps to regulate the immune response and maintain homeostasis during inflammatory stress. (
  • This study bridged this gap by testing whether prenatal social support predicted depressive symptoms at 8 weeks postpartum in a multiethnic sample of 210 women and whether the stress hormone placental corticotropinreleasing hormone (pCRH), measured at 19, 29, and 37 weeks' gestation, mediated this relationship. (
  • Alpha Melanocyte Stimulating Hormone Reverses Corticotropin-Releasing " by Patricia A. Schiml-Webb, Terrence Deak et al. (
  • In particular CRHR1 and CRHR2 activation has been proposed to release endorphin from macrophage/monocytes, granulocytes and lymphocytes of inflamed tissue which in turn desensitizes sensory nerve endings. (
  • These results suggest that CRHR2 expressed on thyrotropes is likely mediating CRH-induced TSH release in altricial avian species like it does in precocial species, and that the increased thyroid hormone levels towards fledging in altricial birds are the result of increased hypothalamic stimulation, in which the thyrotropic activity of CRH may initially play a role. (
  • Proopiomelanocortin, corticotropin releasing hormone and corticotropin releasing hormone receptor genes are expressed in human skin," FEBS Letters, vol. 374, 1999, pp. 113-116. (
  • Corticotropin-releasing hormone (CRH) was infused intracerebroventricularly into rats for 7 d via a miniosmotic pump (1 μg · μl −1 · hr −1 ). (
  • The neuroanatomical substrate of seizures induced by picomolar amounts of corticotropin‐releasing hormone in infant rats was investigated. (
  • Antalarmin inhibits endometriosis progression by corticotropin realizing hormone receptor 1 in rats. (
  • We have shown that hypoxia reduces plasma insulin, which correlates with corticotropin-releasing hormone (CRH) receptor 1 (CRHR1) in rats, but the mechanism remains unclear. (
  • In an attempt to clarify the role of the type 2 corticotropin-releasing hormone (CRH) receptor (CRHR-2) in the brain in activation of the hypothalamic-pituitary-adrenocortical axis, we conducted experiments using male Wistar rats. (
  • Corticotropin releasing hormone promoter polymorphisms in giant cell arteritis and polymyalgia rheumatica. (
  • Based on such hormone loading tests, we diagnosed this patient as idiopathic hypothalamic hypopituitarism and consequent adrenal deficiency. (
  • Each of these parts of the adrenal gland is responsible for producing different types of hormones. (
  • The adrenal gland makes many different hormones and is divided into two distinct zones: the medulla and the cortex. (
  • Diseases of the adrenal gland can often be diagnosed with blood tests that measure the levels of these different hormones, although most adrenal gland disorders affect only the adrenal cortex. (
  • The corticotropin-releasing hormone test can also be used to test adrenal gland function. (
  • A comparison of the effects of human and ovine corticotropin-releasing hormone on the pituitary-adrenal axis. (
  • Cell surface proteins that bind corticotropin-releasing hormone with high affinity and trigger intracellular changes which influence the behavior of cells. (
  • Brain disorders associated with corticotropin-releasing hormone expression in the placenta among children born before the 28th week of gestation. (
  • To evaluate the relationship between placenta corticotropin-releasing hormone (CRH) expression and brain structure and function abnormalities in extremely preterm newborns. (
  • Corticotropin-releasing hormone (CRH) is widely distributed throughout the brain and acts as a putative neurotransmitter/modulator within the CNS. (
  • The ovarian steroid hormone 17β-estradiol acts on central substrates to preserve nerve cell energy stability brain-wide, thereby providing neuroprotection against bio-energetic insults such as neurodegenerative diseases and acute brain ischemia. (
  • It is anticipated that new understanding of the mechanistic basis of how estradiol influences metabolic sensory input from this critical brain locus to discrete downstream regulatory network substrates will likely reveal viable new molecular targets for therapeutic simulation of hormone actions that promote positive neuronal metabolic state during acute and recurring hypoglycemia. (
  • Immunohistochemistry of formalin-fixed, paraffin-embedded Human brain, pituitary labelling Corticotropin Releasing Factor Receptor 2 with ab150510 at 8 µg/ml. (
  • Corticotropin-releasing hormone-like immunoreactivity (CRH-IR) was measured in control and Huntington's disease brain tissues obtained postmortem. (
  • In thyrotropin-releasing hormone (TRH) load test, TSH and prolactin were normally secreted in response to TRH. (
  • Thyrotropin-releasing hormone (TRH) load test: after intravenous injection of TRH (0.5 mg), TSH and PRL levels were examined. (
  • Its release is stimulated by glucocorticoids and catecholamines, which increase prior to parturition lifting this progesterone block. (
  • The authors tested the relationship between genotype at 16 candidate HPA axis single-nucleotide polymorphisms (SNPs) and treatment outcomes for three commonly used antidepressants (escitalopram, sertraline, and extended-release venlafaxine), using multivariable linear and logistic regression with Bonferroni correction. (
  • Estradiol-Dependent Stimulation and Suppression of Gonadotropin-Releasing Hormone Neuron Firing. (
  • Mast cells are necessary for the development of allergic reactions and release numerous vasoactive molecules and cytokines ( Galli, 1993 ). (
  • Luteinizing hormone-releasing hormone (LHRH) load test: after intravenous injection of LHRH (0.1 mg), LH and FSH levels were examined. (
  • Growth hormone releasing hormone (GHRH) load test: after intravenous injection of GHRH (0.1 mg), GH level was examined. (
  • Characterization of corticotropin-releasing hormone (CRH) in human skin," J. Clin. (
  • If 11β-HSD1 was not supposed to be expressed in INS-1 cells, especially if a nonconventional enzyme assay has been used, the result of Fig. 6 C showing corticotropin-releasing hormone-induced inhibition also becomes questionable. (
  • Inhibition of Mouse Melanoma Cell Proliferation by Corticotropin-Releasing Hormone and its Analogs," AntiCancer Research, 21: 1173-1180 (2001). (
  • Placental Corticotropin-Releasing Hormone Mediates the Association Bet" by Jennifer Hahn-Holbrook, Christine Dunkel Schetter et al. (
  • Comparative Immunohistochemistry of Placental Corticotropin-Relea. (
  • However, just after taking hydrocortisone, vomiting was often observed which disturbed sufficient steroid hormone replacement, leading to recurrent hypoglycemia. (
  • Also, we should be aware that hydrocortisone could induce gastrointestinal symptom and that in such a case we should stop hydrocortisone and start prednisolone to sufficiently replace steroid hormone and avoid recurrent hypoglycemia. (
  • I have added today 25mg of DHEA, a steroid hormone, in which I recently showed a relatively low level. (
  • The cortex primarily makes the hormones cortisol and aldosterone. (
  • Impaired basal and restraint-induced epinephrine secretion in corticotropin-releasing hormone-deficient mice. (
  • Evidence that norepinephrine and epinephrine systems mediate the stimulatory effects of ovarian hormones on luteinizing hormone and luteinizing hormone-releasing hormone. (
  • The influence of an upstream open reading frame (ORF) in the 5′-untranslated region (UTR) of the mRNA on corticotropin-releasing hormone receptor type 1 (CRHR1) translation was studied in constructs containing the 5′-UTR of CRHR1, with or without an ATG-to-ATA mutation in the upstream ORF, and the main ORF of luciferase or CRHR1. (
  • Transfection of CRHR1 constructs containing the upstream mutation into AtT20 or LVIP2.0zc reporter cells, resulted in higher 125 I-Tyr-oCRH binding and corticotropin-releasing hormone-stimulated cAMP production, without changes in CRHR1 mRNA levels (measured by RNase protection assay). (
  • Dysfunction of the corticotropin releasing hormone (CRH) and its receptor (CRHR1) system in limbic structures has been implicated in the pathogenesis and course of psychiatric disorders including depression and anxiety. (
  • The transcription factor RelB-NFκB2, activated by the noncanonical NFκB pathway, positively regulates corticotropin-releasing hormone (CRH) and prostaglandin production in the term human placenta and may play an important role in the timing of human parturition. (
  • The ovine corticotropin-releasing hormone (CRH) stimulation test is superior to the human CRH stimulation test for the diagnosis of Cushing's disease. (