Brain-Derived Neurotrophic Factor: A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)Ciliary Neurotrophic Factor: A neurotrophic factor that promotes the survival of various neuronal cell types and may play an important role in the injury response in the nervous system.Glial Cell Line-Derived Neurotrophic Factor: The founding member of the glial cell line-derived neurotrophic factor family. It was originally characterized as a NERVE GROWTH FACTOR promoting the survival of MIDBRAIN dopaminergic NEURONS, and it has been studied as a potential treatment for PARKINSON DISEASE.Nerve Growth Factors: Factors which enhance the growth potentialities of sensory and sympathetic nerve cells.Receptor, Ciliary Neurotrophic Factor: Cell surface receptors for CILIARY NEUROTROPHIC FACTOR. They are heterotrimeric proteins formed by the association of the CILIARY NEUROTROPHIC FACTOR RECEPTOR ALPHA SUBUNIT with the LEUKEMIA INHIBITORY FACTOR RECEPTOR ALPHA SUBUNIT and the CYTOKINE RECEPTOR GP130. Although the receptor regulates neuronal development, it is structurally similar to the cytokine receptor for INTERLEUKIN-6; (RECEPTORS, INTERLEUKIN-6).Receptor, trkB: A protein-tyrosine kinase receptor that is specific for BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; neurotrophin 4 and neurotrophin 5. It is widely expressed in nervous tissue and plays a role in mediating the effects of neurotrophins on growth and differentiation of neuronal cells.Glial Cell Line-Derived Neurotrophic Factor Receptors: A family of GLYCOSYLPHOSPHATIDYLINOSITOL-anchored cell surface receptors that are specific for GLIAL CELL LINE-DERIVED NEUROTROPHIC FACTORS. They form a multi-component receptor complex with PROTO-ONCOGENE PROTEIN C-RET and regulate a variety of intracellular SIGNAL TRANSDUCTION PATHWAYS in conjunction with c-ret protein.Neurotrophin 3: A neurotrophic factor involved in regulating the survival of visceral and proprioceptive sensory neurons. It is closely homologous to nerve growth factor beta and BRAIN-DERIVED NEUROTROPHIC FACTOR.Neurons: 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.Nerve Tissue ProteinsReceptors, Nerve Growth Factor: Cell surface receptors that bind NERVE GROWTH FACTOR; (NGF) and a NGF-related family of neurotrophic factors that includes neurotrophins, BRAIN-DERIVED NEUROTROPHIC FACTOR and CILIARY NEUROTROPHIC FACTOR.Brain Chemistry: Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.Rats, Sprague-Dawley: 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.Brain Injuries: Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.Proto-Oncogene Proteins c-ret: Receptor protein-tyrosine kinases involved in the signaling of GLIAL CELL-LINE DERIVED NEUROTROPHIC FACTOR ligands. They contain an extracellular cadherin domain and form a receptor complexes with GDNF RECEPTORS. Mutations in ret protein are responsible for HIRSCHSPRUNG DISEASE and MULTIPLE ENDOCRINE NEOPLASIA TYPE 2.Hippocampus: A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.Brain: 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.Nerve Growth Factor: NERVE GROWTH FACTOR is the first of a series of neurotrophic factors that were found to influence the growth and differentiation of sympathetic and sensory neurons. It is comprised of alpha, beta, and gamma subunits. The beta subunit is responsible for its growth stimulating activity.Indole Alkaloids: Group of alkaloids containing a benzylpyrrole group (derived from TRYPTOPHAN)Brain Neoplasms: Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.Ciliary Neurotrophic Factor Receptor alpha Subunit: A ciliary neurotrophic factor receptor subunit. It is anchored to the cell surface via GLYCOSYLPHOSPHATIDYLINOSITOL LINKAGE and has specificity for binding to CILIARY NEUROTROPHIC FACTOR. It lacks signal transducing domains which are found on the other two subunits of the receptor.Neuroprotective Agents: Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.Neurturin: A glial cell line-derived neurotrophic factor ligand that is specific for the GFRA2 RECEPTOR. Neurturin is essential for the development of specific postganglionic parasympathetic NEURONS.Cells, Cultured: 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.Neurites: In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell.Cell Survival: The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.Receptor, Nerve Growth Factor: A low affinity receptor that binds NERVE GROWTH FACTOR; BRAIN-DERIVED NEUROTROPHIC FACTOR; NEUROTROPHIN 3; and neurotrophin 4.RNA, Messenger: 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.Brain Mapping: Imaging techniques used to colocalize sites of brain functions or physiological activity with brain structures.Nerve Regeneration: Renewal or physiological repair of damaged nerve tissue.Receptor, trkC: A protein-tyrosine kinase receptor that is specific for NEUROTROPHIN 3. It is widely expressed in nervous tissue and may play a role in mediating the effects of NEUROTROPHIN 3 on the proliferation and differentiation of NEURONS.Receptor Protein-Tyrosine Kinases: A class of cellular receptors that have an intrinsic PROTEIN-TYROSINE KINASE activity.Animals, Newborn: Refers to animals in the period of time just after birth.Cerebral Cortex: The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.Receptor, trkA: A protein-tyrosine kinase receptor that is specific for NERVE GROWTH FACTOR; NEUROTROPHIN 3; neurotrophin 4, neurotrophin 5. It plays a crucial role in pain sensation and thermoregulation in humans. Gene mutations that cause loss of receptor function are associated with CONGENITAL INSENSITIVITY TO PAIN WITH ANHIDROSIS, while gene rearrangements that activate the protein-tyrosine kinase function are associated with tumorigenesis.Disease Models, Animal: 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.Neuronal Plasticity: The capacity of the NERVOUS SYSTEM to change its reactivity as the result of successive activations.Axotomy: Transection or severing of an axon. This type of denervation is used often in experimental studies on neuronal physiology and neuronal death or survival, toward an understanding of nervous system disease.Signal Transduction: 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.Glial Cell Line-Derived Neurotrophic Factors: A family of closely related nerve growth factors that promote NEURON survival. They bind to GDNF RECEPTORS and stimulate SIGNAL TRANSDUCTION through PROTO-ONCOGENE PROTEIN C-RET.Axons: Nerve fibers that are capable of rapidly conducting impulses away from the neuron cell body.Neuroglia: The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Leukemia Inhibitory Factor: An INTERLEUKIN-6 related cytokine that exhibits pleiotrophic effects on many physiological systems that involve cell proliferation, differentiation, and survival. Leukemia inhibitory factor binds to and acts through the lif receptor.Mice, Inbred C57BLBrain Ischemia: Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.Rats, Wistar: A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.Spinal Cord: A cylindrical column of tissue that lies within the vertebral canal. It is composed of WHITE MATTER and GRAY MATTER.Corpus Striatum: Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.Brain Stem: The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.Spiral Ganglion: The sensory ganglion of the COCHLEAR NERVE. The cells of the spiral ganglion send fibers peripherally to the cochlear hair cells and centrally to the COCHLEAR NUCLEI of the BRAIN STEM.Astrocytes: A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.Motor Neurons: Neurons which activate MUSCLE CELLS.Behavior, Animal: The observable response an animal makes to any situation.PC12 Cells: A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.Gene Expression Regulation: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Neurogenesis: Formation of NEURONS which involves the differentiation and division of STEM CELLS in which one or both of the daughter cells become neurons.Substantia Nigra: The black substance in the ventral midbrain or the nucleus of cells containing the black substance. These cells produce DOPAMINE, an important neurotransmitter in regulation of the sensorimotor system and mood. The dark colored MELANIN is a by-product of dopamine synthesis.Dopamine: One of the catecholamine NEUROTRANSMITTERS in the brain. It is derived from TYROSINE and is the precursor to NOREPINEPHRINE and EPINEPHRINE. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (RECEPTORS, DOPAMINE) mediate its action.Receptors, OSM-LIF: Cell surface receptors formed from the dimerization of LIF RECEPTOR ALPHA SUBUNIT with CYTOKINE RECEPTOR GP130. Although originally described as receptors for LEUKEMIA INHIBITORY FACTOR these receptors also bind the closely-related protein ONCOSTATIN M and are referred to as both LIF receptors and type I oncostatin M receptors.Leukemia Inhibitory Factor Receptor alpha Subunit: A receptor subunit that combines with CYTOKINE RECEPTOR GP130 to form the dual specificity receptor for LEUKEMIA INHIBITORY FACTOR and ONCOSTATIN M. The subunit is also a component of the CILIARY NEUROTROPHIC FACTOR RECEPTOR. Both membrane-bound and secreted isoforms of the receptor subunit exist due to ALTERNATIVE SPLICING of its mRNA. The secreted isoform is believed to act as an inhibitory receptor, while the membrane-bound form is a signaling receptor.Tyrosine 3-Monooxygenase: An enzyme that catalyzes the conversion of L-tyrosine, tetrahydrobiopterin, and oxygen to 3,4-dihydroxy-L-phenylalanine, dihydrobiopterin, and water. EC 1.14.16.2.Ganglia, Spinal: Sensory ganglia located on the dorsal spinal roots within the vertebral column. The spinal ganglion cells are pseudounipolar. The single primary branch bifurcates sending a peripheral process to carry sensory information from the periphery and a central branch which relays that information to the spinal cord or brain.Cell Count: The number of CELLS of a specific kind, usually measured per unit volume or area of sample.Carbazoles: Benzo-indoles similar to CARBOLINES which are pyrido-indoles. In plants, carbazoles are derived from indole and form some of the INDOLE ALKALOIDS.Brain Edema: Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Nerve Degeneration: Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Sciatic Nerve: A nerve which originates in the lumbar and sacral spinal cord (L4 to S3) and supplies motor and sensory innervation to the lower extremity. The sciatic nerve, which is the main continuation of the sacral plexus, is the largest nerve in the body. It has two major branches, the TIBIAL NERVE and the PERONEAL NERVE.Magnetic Resonance Imaging: Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.Neurons, Afferent: Neurons which conduct NERVE IMPULSES to the CENTRAL NERVOUS SYSTEM.Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.In Situ Hybridization: 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.Glial Fibrillary Acidic Protein: An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.Cell Differentiation: Progressive restriction of the developmental potential and increasing specialization of function that leads to the formation of specialized cells, tissues, and organs.Schwann Cells: Neuroglial cells of the peripheral nervous system which form the insulating myelin sheaths of peripheral axons.Mesencephalon: The middle of the three primitive cerebral vesicles of the embryonic brain. Without further subdivision, midbrain develops into a short, constricted portion connecting the PONS and the DIENCEPHALON. Midbrain contains two major parts, the dorsal TECTUM MESENCEPHALI and the ventral TEGMENTUM MESENCEPHALI, housing components of auditory, visual, and other sensorimoter systems.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Synapses: Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.Blotting, Western: Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.Cytokine Receptor gp130: A cytokine receptor that acts through the formation of oligomeric complexes of itself with a variety of CYTOKINE RECEPTORS.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Choline O-Acetyltransferase: An enzyme that catalyzes the formation of acetylcholine from acetyl-CoA and choline. EC 2.3.1.6.Oxidopamine: A neurotransmitter analogue that depletes noradrenergic stores in nerve endings and induces a reduction of dopamine levels in the brain. Its mechanism of action is related to the production of cytolytic free-radicals.Dendrites: Extensions of the nerve cell body. They are short and branched and receive stimuli from other NEURONS.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Axonal Transport: The directed transport of ORGANELLES and molecules along nerve cell AXONS. Transport can be anterograde (from the cell body) or retrograde (toward the cell body). (Alberts et al., Molecular Biology of the Cell, 3d ed, pG3)Retina: The ten-layered nervous tissue membrane of the eye. It is continuous with the OPTIC NERVE and receives images of external objects and transmits visual impulses to the brain. Its outer surface is in contact with the CHOROID and the inner surface with the VITREOUS BODY. The outer-most layer is pigmented, whereas the inner nine layers are transparent.Blood-Brain Barrier: Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.Stem Cells: Relatively undifferentiated cells that retain the ability to divide and proliferate throughout postnatal life to provide progenitor cells that can differentiate into specialized cells.Molecular Sequence Data: 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.Cell Death: The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.Cyclic AMP Response Element-Binding Protein: A protein that has been shown to function as a calcium-regulated transcription factor as well as a substrate for depolarization-activated CALCIUM-CALMODULIN-DEPENDENT PROTEIN KINASES. This protein functions to integrate both calcium and cAMP signals.Retinal Ganglion Cells: Neurons of the innermost layer of the retina, the internal plexiform layer. They are of variable sizes and shapes, and their axons project via the OPTIC NERVE to the brain. A small subset of these cells act as photoreceptors with projections to the SUPRACHIASMATIC NUCLEUS, the center for regulating CIRCADIAN RHYTHM.Dose-Response Relationship, Drug: The relationship between the dose of an administered drug and the response of the organism to the drug.Reverse Transcriptase Polymerase Chain Reaction: A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.Growth Inhibitors: Endogenous or exogenous substances which inhibit the normal growth of human and animal cells or micro-organisms, as distinguished from those affecting plant growth (= PLANT GROWTH REGULATORS).Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Antidepressive Agents: Mood-stimulating drugs used primarily in the treatment of affective disorders and related conditions. Several MONOAMINE OXIDASE INHIBITORS are useful as antidepressants apparently as a long-term consequence of their modulation of catecholamine levels. The tricyclic compounds useful as antidepressive agents (ANTIDEPRESSIVE AGENTS, TRICYCLIC) also appear to act through brain catecholamine systems. A third group (ANTIDEPRESSIVE AGENTS, SECOND-GENERATION) is a diverse group of drugs including some that act specifically on serotonergic systems.Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.Chick Embryo: The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.Brain Abscess: A circumscribed collection of purulent exudate in the brain, due to bacterial and other infections. The majority are caused by spread of infected material from a focus of suppuration elsewhere in the body, notably the PARANASAL SINUSES, middle ear (see EAR, MIDDLE); HEART (see also ENDOCARDITIS, BACTERIAL), and LUNG. Penetrating CRANIOCEREBRAL TRAUMA and NEUROSURGICAL PROCEDURES may also be associated with this condition. Clinical manifestations include HEADACHE; SEIZURES; focal neurologic deficits; and alterations of consciousness. (Adams et al., Principles of Neurology, 6th ed, pp712-6)Enzyme-Linked Immunosorbent Assay: An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.Neuropeptides: Peptides released by NEURONS as intercellular messengers. Many neuropeptides are also hormones released by non-neuronal cells.Prosencephalon: The anterior of the three primitive cerebral vesicles of the embryonic brain arising from the NEURAL TUBE. It subdivides to form DIENCEPHALON and TELENCEPHALON. (Stedmans Medical Dictionary, 27th ed)Cerebellum: The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.Memory: Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory.Injections, Intraventricular: Injections into the cerebral ventricles.Synaptic Transmission: The communication from a NEURON to a target (neuron, muscle, or secretory cell) across a SYNAPSE. In chemical synaptic transmission, the presynaptic neuron releases a NEUROTRANSMITTER that diffuses across the synaptic cleft and binds to specific synaptic receptors, activating them. The activated receptors modulate specific ion channels and/or second-messenger systems in the postsynaptic cell. In electrical synaptic transmission, electrical signals are communicated as an ionic current flow across ELECTRICAL SYNAPSES.Optic Nerve Injuries: Injuries to the optic nerve induced by a trauma to the face or head. These may occur with closed or penetrating injuries. Relatively minor compression of the superior aspect of orbit may also result in trauma to the optic nerve. Clinical manifestations may include visual loss, PAPILLEDEMA, and an afferent pupillary defect.Maze Learning: Learning the correct route through a maze to obtain reinforcement. It is used for human or animal populations. (Thesaurus of Psychological Index Terms, 6th ed)Gene Expression Regulation, Developmental: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action during the developmental stages of an organism.Proto-Oncogene Proteins: Products of proto-oncogenes. Normally they do not have oncogenic or transforming properties, but are involved in the regulation or differentiation of cell growth. They often have protein kinase activity.Enzyme Inhibitors: Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.Optic Nerve: The 2nd cranial nerve which conveys visual information from the RETINA to the brain. The nerve carries the axons of the RETINAL GANGLION CELLS which sort at the OPTIC CHIASM and continue via the OPTIC TRACTS to the brain. The largest projection is to the lateral geniculate nuclei; other targets include the SUPERIOR COLLICULI and the SUPRACHIASMATIC NUCLEI. Though known as the second cranial nerve, it is considered part of the CENTRAL NERVOUS SYSTEM.Organ Culture Techniques: A technique for maintenance or growth of animal organs in vitro. It refers to three-dimensional cultures of undisaggregated tissue retaining some or all of the histological features of the tissue in vivo. (Freshney, Culture of Animal Cells, 3d ed, p1)Rats, Long-Evans: An outbred strain of rats developed in 1915 by crossing several Wistar Institute white females with a wild gray male. Inbred strains have been derived from this original outbred strain, including Long-Evans cinnamon rats (RATS, INBRED LEC) and Otsuka-Long-Evans-Tokushima Fatty rats (RATS, INBRED OLETF), which are models for Wilson's disease and non-insulin dependent diabetes mellitus, respectively.Embryo, Mammalian: The entity of a developing mammal (MAMMALS), generally from the cleavage of a ZYGOTE to the end of embryonic differentiation of basic structures. For the human embryo, this represents the first two months of intrauterine development preceding the stages of the FETUS.Synaptophysin: A MARVEL domain-containing protein found in the presynaptic vesicles of NEURONS and NEUROENDOCRINE CELLS. It is commonly used as an immunocytochemical marker for neuroendocrine differentiation.Mice, Mutant Strains: Mice bearing mutant genes which are phenotypically expressed in the animals.1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine: A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.Spinal Cord Injuries: Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).Recombinant Proteins: Proteins prepared by recombinant DNA technology.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Genetic Vectors: DNA molecules capable of autonomous replication within a host cell and into which other DNA sequences can be inserted and thus amplified. Many are derived from PLASMIDS; BACTERIOPHAGES; or VIRUSES. They are used for transporting foreign genes into recipient cells. Genetic vectors possess a functional replicator site and contain GENETIC MARKERS to facilitate their selective recognition.Neostriatum: The phylogenetically newer part of the CORPUS STRIATUM consisting of the CAUDATE NUCLEUS and PUTAMEN. It is often called simply the striatum.Motor Activity: The physical activity of a human or an animal as a behavioral phenomenon.Facial Nerve: The 7th cranial nerve. The facial nerve has two parts, the larger motor root which may be called the facial nerve proper, and the smaller intermediate or sensory root. Together they provide efferent innervation to the muscles of facial expression and to the lacrimal and SALIVARY GLANDS, and convey afferent information for TASTE from the anterior two-thirds of the TONGUE and for TOUCH from the EXTERNAL EAR.Spirostans: Cholestane derivatives containing a fused lactone ring at the 16,17-position and a spiroglycosidic linkage at C-22. Members include sarsaponin, DIOSGENIN and yamogenin.Helplessness, Learned: Learned expectation that one's responses are independent of reward and, hence, do not predict or control the occurrence of rewards. Learned helplessness derives from a history, experimentally induced or naturally occurring, of having received punishment/aversive stimulation regardless of responses made. Such circumstances result in an impaired ability to learn. Used for human or animal populations. (APA, Thesaurus of Psychological Index Terms, 1994)Alzheimer Disease: A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)Recovery of Function: A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.Nodose Ganglion: The inferior (caudal) ganglion of the vagus (10th cranial) nerve. The unipolar nodose ganglion cells are sensory cells with central projections to the medulla and peripheral processes traveling in various branches of the vagus nerve.Central Nervous System: The main information-processing organs of the nervous system, consisting of the brain, spinal cord, and meninges.Neurodegenerative Diseases: Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.Tissue Distribution: Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.Peripheral Nerves: The nerves outside of the brain and spinal cord, including the autonomic, cranial, and spinal nerves. Peripheral nerves contain non-neuronal cells and connective tissue as well as axons. The connective tissue layers include, from the outside to the inside, the epineurium, the perineurium, and the endoneurium.Nerve Crush: Treatment of muscles and nerves under pressure as a result of crush injuries.Apoptosis: One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.Fibroblast Growth Factor 2: A single-chain polypeptide growth factor that plays a significant role in the process of WOUND HEALING and is a potent inducer of PHYSIOLOGIC ANGIOGENESIS. Several different forms of the human protein exist ranging from 18-24 kDa in size due to the use of alternative start sites within the fgf-2 gene. It has a 55 percent amino acid residue identity to FIBROBLAST GROWTH FACTOR 1 and has potent heparin-binding activity. The growth factor is an extremely potent inducer of DNA synthesis in a variety of cell types from mesoderm and neuroectoderm lineages. It was originally named basic fibroblast growth factor based upon its chemical properties and to distinguish it from acidic fibroblast growth factor (FIBROBLAST GROWTH FACTOR 1).Dentate Gyrus: GRAY MATTER situated above the GYRUS HIPPOCAMPI. It is composed of three layers. The molecular layer is continuous with the HIPPOCAMPUS in the hippocampal fissure. The granular layer consists of closely arranged spherical or oval neurons, called GRANULE CELLS, whose AXONS pass through the polymorphic layer ending on the DENDRITES of PYRAMIDAL CELLS in the hippocampus.Amino Acid Sequence: 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.Dendritic Spines: Spiny processes on DENDRITES, each of which receives excitatory input from one nerve ending (NERVE ENDINGS). They are commonly found on PURKINJE CELLS and PYRAMIDAL CELLS.Ganglia, Sensory: Clusters of neurons in the somatic peripheral nervous system which contain the cell bodies of sensory nerve axons. Sensory ganglia may also have intrinsic interneurons and non-neuronal supporting cells.Parkinson Disease, Secondary: Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)Oncostatin M: A cytokine with both pro- and anti-inflammatory actions that depend upon the cellular microenvironment. Oncostatin M is a 28 kDa monomeric glycoprotein that is similar in structure to LEUKEMIA INHIBITORY FACTOR. Its name derives from the the observation that it inhibited the growth of tumor cells and augmented the growth of normal fibroblasts.Parkinson Disease: A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)Culture Media, Conditioned: Culture media containing biologically active components obtained from previously cultured cells or tissues that have released into the media substances affecting certain cell functions (e.g., growth, lysis).Base Sequence: The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.Neurotoxins: Toxic substances from microorganisms, plants or animals that interfere with the functions of the nervous system. Most venoms contain neurotoxic substances. Myotoxins are included in this concept.Ganglia, Sympathetic: Ganglia of the sympathetic nervous system including the paravertebral and the prevertebral ganglia. Among these are the sympathetic chain ganglia, the superior, middle, and inferior cervical ganglia, and the aorticorenal, celiac, and stellate ganglia.Dopaminergic Neurons: Neurons whose primary neurotransmitter is DOPAMINE.Huntington Disease: A familial disorder inherited as an autosomal dominant trait and characterized by the onset of progressive CHOREA and DEMENTIA in the fourth or fifth decade of life. Common initial manifestations include paranoia; poor impulse control; DEPRESSION; HALLUCINATIONS; and DELUSIONS. Eventually intellectual impairment; loss of fine motor control; ATHETOSIS; and diffuse chorea involving axial and limb musculature develops, leading to a vegetative state within 10-15 years of disease onset. The juvenile variant has a more fulminant course including SEIZURES; ATAXIA; dementia; and chorea. (From Adams et al., Principles of Neurology, 6th ed, pp1060-4)Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.Neural Pathways: Neural tracts connecting one part of the nervous system with another.Green Fluorescent Proteins: Protein analogs and derivatives of the Aequorea victoria green fluorescent protein that emit light (FLUORESCENCE) when excited with ULTRAVIOLET RAYS. They are used in REPORTER GENES in doing GENETIC TECHNIQUES. Numerous mutants have been made to emit other colors or be sensitive to pH.Kainic Acid: (2S-(2 alpha,3 beta,4 beta))-2-Carboxy-4-(1-methylethenyl)-3-pyrrolidineacetic acid. Ascaricide obtained from the red alga Digenea simplex. It is a potent excitatory amino acid agonist at some types of excitatory amino acid receptors and has been used to discriminate among receptor types. Like many excitatory amino acid agonists it can cause neurotoxicity and has been used experimentally for that purpose.Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.Brain Infarction: Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.Hypoxia, Brain: A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.Trigeminal Ganglion: The semilunar-shaped ganglion containing the cells of origin of most of the sensory fibers of the trigeminal nerve. It is situated within the dural cleft on the cerebral surface of the petrous portion of the temporal bone and gives off the ophthalmic, maxillary, and part of the mandibular nerves.Rats, Inbred F344Spermatogonia: Euploid male germ cells of an early stage of SPERMATOGENESIS, derived from prespermatogonia. With the onset of puberty, spermatogonia at the basement membrane of the seminiferous tubule proliferate by mitotic then meiotic divisions and give rise to the haploid SPERMATOCYTES.Denervation: The resection or removal of the nerve to an organ or part. (Dorland, 28th ed)Long-Term Potentiation: A persistent increase in synaptic efficacy, usually induced by appropriate activation of the same synapses. The phenomenological properties of long-term potentiation suggest that it may be a cellular mechanism of learning and memory.Receptors, Cytokine: Cell surface proteins that bind cytokines and trigger intracellular changes influencing the behavior of cells.Gene Transfer Techniques: The introduction of functional (usually cloned) GENES into cells. A variety of techniques and naturally occurring processes are used for the gene transfer such as cell hybridization, LIPOSOMES or microcell-mediated gene transfer, ELECTROPORATION, chromosome-mediated gene transfer, TRANSFECTION, and GENETIC TRANSDUCTION. Gene transfer may result in genetically transformed cells and individual organisms.Swimming: An activity in which the body is propelled through water by specific movement of the arms and/or the legs. Swimming as propulsion through water by the movement of limbs, tail, or fins of animals is often studied as a form of PHYSICAL EXERTION or endurance.Neuroblastoma: A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)Transfection: The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.Autoradiography: The making of a radiograph of an object or tissue by recording on a photographic plate the radiation emitted by radioactive material within the object. (Dorland, 27th ed)Drosophila Proteins: Proteins that originate from insect species belonging to the genus DROSOPHILA. The proteins from the most intensely studied species of Drosophila, DROSOPHILA MELANOGASTER, are the subject of much interest in the area of MORPHOGENESIS and development.Hypothalamus: 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.Extracellular Signal-Regulated MAP Kinases: A mitogen-activated protein kinase subfamily that is widely expressed and plays a role in regulation of MEIOSIS; MITOSIS; and post mitotic functions in differentiated cells. The extracellular signal regulated MAP kinases are regulated by a broad variety of CELL SURFACE RECEPTORS and can be activated by certain CARCINOGENS.Enteric Nervous System: Two ganglionated neural plexuses in the gut wall which form one of the three major divisions of the autonomic nervous system. The enteric nervous system innervates the gastrointestinal tract, the pancreas, and the gallbladder. It contains sensory neurons, interneurons, and motor neurons. Thus the circuitry can autonomously sense the tension and the chemical environment in the gut and regulate blood vessel tone, motility, secretions, and fluid transport. The system is itself governed by the central nervous system and receives both parasympathetic and sympathetic innervation. (From Kandel, Schwartz, and Jessel, Principles of Neural Science, 3d ed, p766)Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.Physical Conditioning, Animal: Diet modification and physical exercise to improve the ability of animals to perform physical activities.Oligodendroglia: A class of large neuroglial (macroglial) cells in the central nervous system. Oligodendroglia may be called interfascicular, perivascular, or perineuronal (not the same as SATELLITE CELLS, PERINEURONAL of GANGLIA) according to their location. They form the insulating MYELIN SHEATH of axons in the central nervous system.GAP-43 Protein: A nervous tissue specific protein which is highly expressed in NEURONS during development and NERVE REGENERATION. It has been implicated in neurite outgrowth, long-term potentiation, SIGNAL TRANSDUCTION, and NEUROTRANSMITTER release. (From Neurotoxicology 1994;15(1):41-7) It is also a substrate of PROTEIN KINASE C.Injections: Introduction of substances into the body using a needle and syringe.Receptors, N-Methyl-D-Aspartate: A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.Stilbamidines: STILBENES with AMIDINES attached.Retinal Degeneration: A retrogressive pathological change in the retina, focal or generalized, caused by genetic defects, inflammation, trauma, vascular disease, or aging. Degeneration affecting predominantly the macula lutea of the retina is MACULAR DEGENERATION. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p304)Corticosterone: 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)Geniculate Ganglion: The sensory ganglion of the facial (7th cranial) nerve. The geniculate ganglion cells send central processes to the brain stem and peripheral processes to the taste buds in the anterior tongue, the soft palate, and the skin of the external auditory meatus and the mastoid process.gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.Amygdala: 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.Diazinon: A cholinesterase inhibitor that is used as an organothiophosphorus insecticide.Photoreceptor Cells, Vertebrate: Specialized PHOTOTRANSDUCTION neurons in the vertebrates, such as the RETINAL ROD CELLS and the RETINAL CONE CELLS. Non-visual photoreceptor neurons have been reported in the deep brain, the PINEAL GLAND and organs of the circadian system.Myelin Sheath: The lipid-rich sheath surrounding AXONS in both the CENTRAL NERVOUS SYSTEMS and PERIPHERAL NERVOUS SYSTEM. The myelin sheath is an electrical insulator and allows faster and more energetically efficient conduction of impulses. The sheath is formed by the cell membranes of glial cells (SCHWANN CELLS in the peripheral and OLIGODENDROGLIA in the central nervous system). Deterioration of the sheath in DEMYELINATING DISEASES is a serious clinical problem.Coculture Techniques: A technique of culturing mixed cell types in vitro to allow their synergistic or antagonistic interactions, such as on CELL DIFFERENTIATION or APOPTOSIS. Coculture can be of different types of cells, tissues, or organs from normal or disease states.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Cognition: Intellectual or mental process whereby an organism obtains knowledge.Amyloid beta-Peptides: Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.Frontal Lobe: The part of the cerebral hemisphere anterior to the central sulcus, and anterior and superior to the lateral sulcus.Sensory Receptor Cells: Specialized afferent neurons capable of transducing sensory stimuli into NERVE IMPULSES to be transmitted to the CENTRAL NERVOUS SYSTEM. Sometimes sensory receptors for external stimuli are called exteroceptors; for internal stimuli are called interoceptors and proprioceptors.Rhizotomy: Surgical interruption of a spinal or cranial nerve root. (From Dorland, 28th ed)Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.Microglia: The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.

Expression of the naturally occurring truncated trkB neurotrophin receptor induces outgrowth of filopodia and processes in neuroblastoma cells. (1/3019)

We have investigated the effects of the truncated trkB receptor isoform T1 (trkB.T1) by transient transfection into mouse N2a neuroblastoma cells. We observed that expression of trkB.T1 leads to a striking change in cell morphology characterized by outgrowth of filopodia and processes. A similar morphological response was also observed in SH-SY5Y human neuroblastoma cells and NIH3T3 fibroblasts transfected with trkB.T1. N2a cells lack endogenous expression of trkB isoforms, but express barely detectable amounts of its ligands, brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4). The morphological change was ligand-independent, since addition of exogenous BDNF or NT-4 or blockade of endogenous trkB ligands did not influence this response. Filopodia and process outgrowth was significantly suppressed when full-length trkB.TK+ was cotransfected together with trkB.T1 and this inhibitory effect was blocked by tyrosine kinase inhibitor K252a. Transfection of trkB.T1 deletion mutants showed that the morphological response is dependent on the extracellular, but not the intracellular domain of the receptor. Our results suggest a novel ligand-independent role for truncated trkB in the regulation of cellular morphology.  (+info)

Activated macrophages and microglia induce dopaminergic sprouting in the injured striatum and express brain-derived neurotrophic factor and glial cell line-derived neurotrophic factor. (2/3019)

Nigrostriatal dopaminergic neurons undergo sprouting around the margins of a striatal wound. The mechanism of this periwound sprouting has been unclear. In this study, we have examined the role played by the macrophage and microglial response that follows striatal injury. Macrophages and activated microglia quickly accumulate after injury and reach their greatest numbers in the first week. Subsequently, the number of both cell types declines rapidly in the first month and thereafter more slowly. Macrophage numbers eventually cease to decline, and a sizable group of these cells remains at the wound site and forms a long-term, highly activated resident population. This population of macrophages expresses increasing amounts of glial cell line-derived neurotrophic factor mRNA with time. Brain-derived neurotrophic factor mRNA is also expressed in and around the wound site. Production of this factor is by both activated microglia and, to a lesser extent, macrophages. The production of these potent dopaminergic neurotrophic factors occurs in a similar spatial distribution to sprouting dopaminergic fibers. Moreover, dopamine transporter-positive dopaminergic neurites can be seen growing toward and embracing hemosiderin-filled wound macrophages. The dopaminergic sprouting that accompanies striatal injury thus appears to result from neurotrophic factor secretion by activated macrophages and microglia at the wound site.  (+info)

BDNF mediates the effects of testosterone on the survival of new neurons in an adult brain. (3/3019)

New neurons are incorporated into the high vocal center (HVC), a nucleus of the adult canary (Serinus canaria) brain that plays a critical role in the acquisition and production of learned song. Recruitment of new neurons in the HVC is seasonally regulated and depends upon testosterone levels. We show here that brain-derived neurotrophic factor (BDNF) is present in the HVC of adult males but is not detectable in that of females, though the HVC of both sexes has BDNF receptors (TrkB). Testosterone treatment increases the levels of BDNF protein in the female HVC, and BDNF infused into the HVC of adult females triples the number of new neurons. Infusion of a neutralizing antibody to BDNF blocks the testosterone-induced increase in new neurons. Our results demonstrate that BDNF is involved in the regulation of neuronal replacement in the adult canary brain and suggest that the effects of testosterone are mediated through BDNF.  (+info)

Activated human T cells, B cells, and monocytes produce brain-derived neurotrophic factor in vitro and in inflammatory brain lesions: a neuroprotective role of inflammation? (4/3019)

Brain-derived neurotrophic factor (BDNF) has potent effects on neuronal survival and plasticity during development and after injury. In the nervous system, neurons are considered the major cellular source of BDNF. We demonstrate here that in addition, activated human T cells, B cells, and monocytes secrete bioactive BDNF in vitro. Notably, in T helper (Th)1- and Th2-type CD4(+) T cell lines specific for myelin autoantigens such as myelin basic protein or myelin oligodendrocyte glycoprotein, BDNF production is increased upon antigen stimulation. The BDNF secreted by immune cells is bioactive, as it supports neuronal survival in vitro. Using anti-BDNF monoclonal antibody and polyclonal antiserum, BDNF immunoreactivity is demonstrable in inflammatory infiltrates in the brain of patients with acute disseminated encephalitis and multiple sclerosis. The results raise the possibility that in the nervous system, inflammatory infiltrates have a neuroprotective effect, which may limit the success of nonselective immunotherapies.  (+info)

Growth factor-mediated Fyn signaling regulates alpha-amino-3- hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor expression in rodent neocortical neurons. (5/3019)

Src-family protein tyrosine kinases (PTKs) transduce signals to regulate neuronal development and synaptic plasticity. However, the nature of their activators and molecular mechanisms underlying these neural processes are unknown. Here, we show that brain-derived neurotrophic factor (BDNF) and platelet-derived growth factor enhance expression of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptor 1 and 2/3 proteins in rodent neocortical neurons via the Src-family PTK(s). The increase in AMPA receptor levels was blocked in cultured neocortical neurons by addition of a Src-family-selective PTK inhibitor. Accordingly, neocortical cultures from Fyn-knockout mice failed to respond to BDNF whereas those from wild-type mice responded. Moreover, the neocortex of young Fyn mutants exhibited a significant in vivo reduction in these AMPA receptor proteins but not in their mRNA levels. In vitro kinase assay revealed that BDNF can indeed activate the Fyn kinase: It enhanced tyrosine phosphorylation of Fyn as well as that of enolase supplemented exogenously. All of these results suggest that the Src-family kinase Fyn, activated by the growth factors, plays a crucial role in modulating AMPA receptor expression during brain development.  (+info)

Differential sorting of nerve growth factor and brain-derived neurotrophic factor in hippocampal neurons. (6/3019)

Nerve growth factor (NGF) is released through the constitutive secretory pathway from cells in peripheral tissues and nerves where it can act as a target-derived survival factor. In contrast, brain-derived neurotrophic factor (BDNF) appears to be processed in the regulated secretory pathway of brain neurons and secreted in an activity-dependent manner to play a role in synaptic plasticity. To determine whether sorting differences are intrinsic to the neurotrophins or reflect differences between cell types, we compared NGF and BDNF processing in cultured hippocampal neurons using a Vaccinia virus expression system. Three independent criteria (retention or release from cells after pulse-chase labeling, depolarization-dependent release, and immunocytochemical localization) suggest that the bulk of newly synthesized NGF is sorted into the constitutive pathway, whereas BDNF is primarily sorted into the regulated secretory pathway. Similar results occurred with AtT 20 cells, including those transfected with cDNAs encoding neurotrophin precursor-green fluorescent protein fusions. The NGF precursor, but not the BDNF precursor, is efficiently cleaved by the endoprotease furin in the trans-Golgi network (TGN). Blocking furin activity in AtT 20 cells with alpha1-PDX as well as increasing the expression of NGF precursor partially directed NGF into the regulated secretory pathway. Therefore, neurotrophins can be sorted into either the constitutive or regulated secretory pathways, and sorting may be regulated by the efficiency of furin cleavage in the TGN. This mechanism may explain how neuron-generated neurotrophins can act both as survival factors and as neuropeptides.  (+info)

Brain-derived neurotrophic factor prevents low-frequency inputs from inducing long-term depression in the developing visual cortex. (7/3019)

Brain-derived neurotrophic factor (BDNF) is reported to enhance synaptic transmission and to play a role in long-term potentiation in hippocampus and neocortex. If so, a shortage or blockade of BDNF might lead to another form of synaptic plasticity, long-term depression (LTD). To test this possibility and to elucidate mechanisms if it is the case, EPSCs evoked by test stimulation of layer IV were recorded from layer II/III neurons in visual cortical slices of young rats in the whole-cell voltage-clamp mode. LTD was induced by low-frequency stimulation (LFS) at 1 Hz for 10-15 min if each pulse of the LFS was paired with depolarization of neurons to -30 mV but was not induced if their membrane potentials were kept at -70 mV. Such an LTD was blocked by exogenously applied BDNF, probably through presynaptic mechanisms. Suppression of endogenous BDNF activity by the anti-BDNF antibody or an inhibitor for BDNF receptors made otherwise ineffective stimuli (LFS without postsynaptic depolarization) effective for LTD induction, suggesting that endogenous BDNF may prevent low-frequency inputs from inducing LTD in the developing visual cortex.  (+info)

BDNF is a target-derived survival factor for arterial baroreceptor and chemoafferent primary sensory neurons. (8/3019)

Brain-derived neurotrophic factor (BDNF) supports survival of 50% of visceral afferent neurons in the nodose/petrosal sensory ganglion complex (NPG; Ernfors et al., 1994a; Jones et al., 1994; Conover et al., 1995; Liu et al., 1995; Erickson et al., 1996), including arterial chemoafferents that innervate the carotid body and are required for development of normal breathing (Erickson et al., 1996). However, the relationship between BDNF dependence of visceral afferents and the location and timing of BDNF expression in visceral tissues is unknown. The present study demonstrates that BDNF mRNA and protein are transiently expressed in NPG targets in the fetal cardiac outflow tract, including baroreceptor regions in the aortic arch, carotid sinus, and right subclavian artery, as well as in the carotid body. The period of BDNF expression corresponds to the onset of sensory innervation and to the time at which fetal NPG neurons are BDNF-dependent in vitro. Moreover, baroreceptor innervation is absent in newborn mice lacking BDNF. In addition to vascular targets, vascular afferents themselves express high levels of BDNF, both during and after the time they are BDNF-dependent. However, endogenous BDNF supports survival of fetal NPG neurons in vitro only under depolarizing conditions. Together, these data indicate two roles for BDNF during vascular afferent pathway development; initially, as a target-derived survival factor, and subsequently, as a signaling molecule produced by the afferents themselves. Furthermore, the fact that BDNF is required for survival of functionally distinct populations of vascular afferents demonstrates that trophic requirements of NPG neurons are not modality-specific but may instead be associated with innervation of particular organ systems.  (+info)

*Epigenetics of neurodegenerative diseases

... a brain-derived neurotrophic factor that function in nerve growth and maintenance within the brain.[86][20]. *Vorinostat (SAHA) ... a neurotrophic factor important for long-term memory.[66] Expression of CREB, an activity-dependent transcription factor ... but are reduced in PD brain.[89]. DNA methylation. Neurons of PD patients show hypomethylation of tumor necrosis factor (TNF) ... in human AD brain, while other studies have shown upregulation or downregulation of miRNA-9 in brain.[61]. DNA methylation. In ...

*Neurotrophin-4

"Sortilin controls intracellular sorting of brain-derived neurotrophic factor to the regulated secretory pathway". J. Neurosci. ... Götz R, Schartl M (1994). "The conservation of neurotrophic factors during vertebrate evolution". Comp Biochem Physiol ... 2008). "Association study of 10 genes encoding neurotrophic factors and their receptors in adult and child attention-deficit/ ... It is a neurotrophic factor that signals predominantly through the TrkB receptor tyrosine kinase. ...

*Rett syndrome

There is an association of the disease[which?] with brain-derived neurotrophic factor (BDNF). An interactive pathway map of ... Brain levels of norepinephrine are lower in people with Rett syndrome (reviewed in). The genetic loss of MECP2 changes the ... In cases of the sporadic form of RTT, the mutated MECP2 is thought to derive almost exclusively from a de novo mutation on the ... Rett syndrome (RTT) is a genetic brain disorder which typically becomes apparent after six months of age in females. Symptoms ...

*Neurotrophin

Brain-derived neurotrophic factor[edit]. Main article: Brain-derived neurotrophic factor. Brain-derived neurotrophic factor ( ... brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4).[6] The term neurotrophic factor ... "Regional distribution of brain-derived neurotrophic factor mRNA in the adult mouse brain". EMBO J. 9 (8): 2459-2464. PMC 552273 ... Nerve growth factor[edit]. Main article: Nerve growth factor. Nerve growth factor (NGF), the prototypical growth factor, is a ...

*Neurotrophin

Brain-derived neurotrophic factor[edit]. Main article: Brain-derived neurotrophic factor. Brain-derived neurotrophic factor ( ... brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4 (NT-4).[6] The term neurotrophic factor ... "Regional distribution of brain-derived neurotrophic factor mRNA in the adult mouse brain". The EMBO Journal. 9 (8): 2459-64. ... Nerve growth factor[edit]. Main article: Nerve growth factor. Nerve growth factor (NGF), the prototypical growth factor, is a ...

*CADPS2

This gene interacts with brain-derived neurotrophic factor. Cadps2 has been linked to autism and is in the 7q autism ... French, L.; Pavlidis, P. (6 January 2011). "Relationships between gene expression and brain wiring in the adult rodent brain". ... The complete sequences of 100 new cDNA clones from brain which code for large proteins in vitro". DNA Res. 7 (4): 273-81. doi: ... CADPS2 has been linked to human and mouse brain structure in two large genomic studies. GRCh38: Ensembl release 89: ...

*Biology of depression

Dwivedi Y (2009). "Brain-derived neurotrophic factor: role in depression and suicide". Neuropsychiatr Dis Treat. 5: 433-49. doi ... Instead of studying one brain region, studying large scale brain networks is another approach to understanding psychiatric and ... Sleep deprivation and light therapy both target the same brain neurotransmitter system and brain areas as antidepressant drugs ... The sole source of serotonin in the brain is the raphe nuclei, a group of small nerve cell nuclei in the upper brain stem, ...

*CX614

Lauterborn JC, Truong GS, Baudry M, Bi X, Lynch G, Gall CM (Oct 2003). "Chronic elevation of brain-derived neurotrophic factor ... Chronic CX-614 treatments produce rapid increases in the synthesis of the brain-derived neurotrophic factor BDNF which has very ...

*Perl-UNC Prize

2003 Yves Barde, Discovery of Brain-Derived Neurotrophic Factor. 2004 Roger Tsien, Development of Tools for Monitoring ... 2006 Solomon H. Snyder, Identification of Opiate Receptors in the Brain. 2007 Huda Zoghbi, Discovery of the Genetic Basis of ... 2013 Marcus Raichle, Discoveries Relating to the "Default Mode Network" of Brain Function. 2014 David W. Tank, Discovery of ...

*LINGO1

... brain derived neurotrophic factor (BNDF) and its receptor, amyloid precursor protein (APP), and tropomyosin receptor kinase A ( ... "Interactions between brain-derived neurotrophic factor and the TRKB receptor. Identification of two ligand binding domains in ... Traumatic brain injury involves the necrotic and apoptotic death of brain cells in vulnerable and delicate areas such as the ... Both myelination and neurite outgrowth occur during brain maturation, and it is during this late period of brain development ( ...

*Tropomyosin receptor kinase B

"The neurotrophic factors brain-derived neurotrophic factor and neurotrophin-3 are ligands for the trkB tyrosine kinase receptor ... "trkB encodes a functional receptor for brain-derived neurotrophic factor and neurotrophin-3 but not nerve growth factor". Cell ... "trkB encodes a functional receptor for brain-derived neurotrophic factor and neurotrophin-3 but not nerve growth factor". Cell ... Suzuki S, Mizutani M, Suzuki K, Yamada M, Kojima M, Hatanaka H, Koizumi S (June 2002). "Brain-derived neurotrophic factor ...

*PPP1R1B

Brain-derived neurotrophic factor regulates the expression of DARPP-32. The Akt and CDK5/p35 intracelular pathway is suggested ... "AKT and CDK5/p35 mediate brain-derived neurotrophic factor induction of DARPP-32 in medium size spiny neurons in vitro". J. ... "AKT and CDK5/p35 mediate brain-derived neurotrophic factor induction of DARPP-32 in medium size spiny neurons in vitro". J. ... "Role of phosphatidylinositide 3-kinase in brain-derived neurotrophic factor-induced DARPP-32 expression in medium size spiny ...

*LM22A-4

... the main receptor of brain-derived neurotrophic factor. It has been found to possess poor blood-brain-barrier penetration when ... Gary Lewin; Bruce D. Carter (25 March 2014). Neurotrophic Factors. Springer Science & Business Media. pp. 490-491. ISBN 978-3- ... 189-. ISBN 978-1-4398-2708-6. Numakawa, Tadahiro (2014). "Possible protective action of neurotrophic factors and natural ...

*WAGR syndrome

The gene for brain-derived neurotrophic factor (BDNF), located on 11p14.1, has been proposed as a candidate gene for the ... August 2008). "Brain-derived neurotrophic factor and obesity in the WAGR syndrome". N. Engl. J. Med. 359 (9): 918-27. doi: ... Mutations in the PAX6 gene have recently been shown to not only cause ocular abnormalities, but also problems in the brain and ... "PAX6 mutation as a genetic factor common to aniridia and glucose intolerance". Diabetes. 51 (1): 224-30. doi:10.2337/diabetes. ...

*Neurotrophin-3

NT-3 was the third neurotrophic factor to be characterized, after nerve growth factor (NGF) and BDNF (Brain Derived ... "Nerve Growth Factor") BDNF (for "Brain Derived Neurotrophic Factor") NT-4 (for "Neurotrophin-4") While TrkB mediates the ... Ozçelik T, Rosenthal A, Francke U (1991). "Chromosomal mapping of brain-derived neurotrophic factor and neurotrophin-3 genes in ... Robinson RC, Radziejewski C, Stuart DI, Jones EY (1995). "Structure of the brain-derived neurotrophic factor/neurotrophin 3 ...

*Synaptogenesis

For instance, brain-derived neurotrophic factor (BDNF) is produced by the brain and regulates several functions within the ... June 2007). "Brain-derived neurotrophic factor regulates cholesterol metabolism for synapse development". J. Neurosci. 27 (24 ... Cao G, Ko CP (June 2007). "Schwann cell-derived factors modulate synaptic activities at developing neuromuscular synapses". J. ... This brain region contains three main neuronal cell types- Purkinje cells, granule cells and mossy fiber cells. Wnt-3 ...

*Choroba Alzheimera, wolna encyklopedia

Wymienia się tutaj BDNF (brain derived neurotrophic factor)[75][76].. Genetyka[edytuj]. Olbrzymią większość przypadków AD ... Schindowski K, Belarbi K, Buée L. Neurotrophic factors in Alzheimer's disease: role of axonal transport. „Genes, Brain and ... Brain". 132 (Pt 8), s. 2048-57, 08 2009. DOI: 10.1093/brain/awp123. PMID: 19460794. PMCID: PMC2714061. ... Brain". 131 (Pt 6), s. 1630-45, 06 2008. DOI: 10.1093/brain/awn016. PMID: 18339640. PMCID: PMC2408940. ...

*Bulimia nervosa

Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism.[28][29] ... Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia.[21] In a 1991 study by ... Adolescents are at the stage where their brains are still quite malleable and developing gradually.[66] Therefore, young ... A study dedicated to investigating the thin ideal internalization as a factor of bulimia nervosa is Thompson's and Stice's ...

*Activity-regulated cytoskeleton-associated protein

... including mitogens such as epidermal growth factor (EGF), nerve growth factor (NGF), and brain-derived neurotrophic factor ( ... Yin Y, Edelman GM, Vanderklish PW (2002). "The brain-derived neurotrophic factor enhances synthesis of Arc in synaptoneurosomes ... Several transcription factors are known to be involved in regulating the Arc gene (see above), including serum response factor ... "The serum response factor and a putative novel transcription factor regulate expression of the immediate-early gene Arc/Arg3.1 ...

*5-HT1A receptor

The 5-HT1A receptor has been shown to interact with brain-derived neurotrophic factor (BDNF), which may play a major role in ... "Brain-derived neurotrophic factor-deficient mice exhibit a hippocampal hyperserotonergic phenotype". Int. J. ... Brain Res. 195 (1): 54-77. doi:10.1016/j.bbr.2008.02.023. PMID 18394726. Meltzer HY, Sumiyoshi T (December 2008). "Does ... Brain Res. 195 (1): 98-102. doi:10.1016/j.bbr.2008.05.016. PMID 18707769. Spreitzer H (August 13, 2008). "Neue Wirkstoffe - ...

*Envelope glycoprotein GP120

"Human Immunodeficiency Virus Type 1 Alters Brain-Derived Neurotrophic Factor Processing in Neurons". The Journal of ... "HIV-1 viral proteins gp120 and Tat induce oxidative stress in brain endothelial cells". Brain Res. 1045 (1-2): 57-63. doi: ... and transmigration across the blood-brain barrier: modulatory effects of STAT1 signaling". Microvasc. Res. 77 (2): 212-9. doi: ...

*Bunuh diri bahasa Indonesia, ensiklopedia bebas

Rendahnya tingkat brain-derived neurotrophic factor (BDNF) yang terkait secara langsung dengan bunuh diri[80] dan secara tidak ... Sher, L (2011 May). "Brain-derived neurotrophic factor and suicidal behavior.". QJM : monthly journal of the Association of ... Sher, L (2011). "The role of brain-derived neurotrophic factor in the pathophysiology of adolescent suicidal behavior.". ... Simpson, G; Tate, R (2007 Dec). "Suicidality in people surviving a traumatic brain injury: prevalence, risk factors and ...

*Epigenetics of schizophrenia

BDNF - Brain-derived neurotrophic factor, BDNF, is another important gene in the study of schizophrenia genetics. BDNF plays a ... DNA methylation can also affect expression of BDNF (brain derived neurotrophic factor). The BDNF protein is important for ... Some postmortem brain studies looking at the gene expression of histone methylation has shown promising results that might be ... One of the most common methods is looking at postmortem brain tissue of patients with schizophrenia and analyzing them for ...

*Bulimia nervosa

Brain-derived neurotrophic factor (BDNF) is under investigation as a possible mechanism. There is evidence that sex hormones ... The percentage risk that is estimated to be due to genetics is between 30% and 80%. Other risk factors for the disease include ... Media portrayals of an 'ideal' body shape are widely considered to be a contributing factor to bulimia. In a 1991 study by ... A study dedicated to investigating the thin ideal internalization as a factor of bulimia nervosa is Thompson's and Stice's ...

*Exercise

... increases brain neurotrophic proteins, such as brain-derived neurotrophic factor (BDNF), and prevents cognitive diseases [76-78 ... "A meta-analytic review of the effects of exercise on brain-derived neurotrophic factor". J Psychiatr Res. 60C: 56-64. doi: ... with preliminary evidence suggesting that brain-derived neurotrophic factor (BDNF) may mediate these effects. The aim of the ... and increases neurotrophic factors in different areas of the brain, possibly providing reserve against later cognitive decline ...

*Epigenetics of depression

Brain-derived neurotrophic factor (BDNF) is a neurotrophic growth factor that is important for the growth and survival of ... Brain derived neurotrophic factor (BDNF), which has shown been shown to be downregulated in patients with major depressive ... Decreased brain-derived neurotrophic factor (BDNF) is known to be associated with depression. Research suggests that increasing ... Glial cell-derived neurotrophic factor (GDNF) is a protein that aids in the survival and differentiation of dopaminergic ...

*Substance P

... the role of brain-derived neurotrophic factor and substance P". The British Journal of Dermatology. 157 (5): 922-5. doi:10.1111 ... Donkin JJ, Turner RJ, Hassan I, Vink R (2007). "Substance P in traumatic brain injury". Progress in Brain Research. 161: 97-109 ... Substance P and the NK1 receptor are widely distributed in the brain and are found in brain regions that are specific to ... "Neurotrophic and anhidrotic keratopathy treated with substance P and insulinlike growth factor 1". Archives of Ophthalmology. ...

*Anne Farmer

"Stressful life events and the brain-derived neurotrophic factor gene in bipolar disorder. J Affect Disord. 2010 Feb 19. Hosang ... Current research includes investigating genetic and environmental risk factors for unipolar and bipolar affective disorders, ... "Could genetic risk factors account for the variation in suicide rates seen in European countries?", Zdravstveno varstvo. ...
Researchers have reported that serum brain-derived neurotrophic factor (sBDNF) of drug-free depressed patients are lower than those of healthy controls and proposed that low sBDNF levels might reflect
Experimental evidence in mice indicates that environmental conditions affect females and males differently. However, in a recent study analyzing the heterozygous mutation of brain-derived neurotrophic factor (BDNF), both sexes presented a similar emotional phenotype, which became obvious only under impoverished, but not in enriched conditions suggesting an enrichment-induced rescue. To investigate the basis of this behavioral rescue effect, we analyzed neurochemical changes (BDNF expression, serotonergic changes, and corticosterone) in the hippocampus, frontal cortex and hypothalamus of animals housed under respective conditions. In male mice, enrichment induced an increase of BDNF expression in the hippocampus of both BDNF heterozygous (BDNF(+/-)) and wild-types. Notably, in enriched-reared BDNF(+/-) mice BDNF mRNA and protein increased to levels comparable to those of wild-types in impoverished environment. In the frontal cortex of males, only wild-types presented an enrichment-induced increase of
Exercise is recognized as a promising approach to counteract aging-associated declines in cognitive functions. However, the exact molecular pathways involved remain unclear. Aerobic training interventions and improvements in peak oxygen uptake (VO2peak) have been associated with increases in the peripheral concentration of brain-derived neurotrophic factor (BDNF) and better cognitive performances. However, other training interventions such as resistance training and gross motor skills programs were also linked with improvements in cognitive functions. Thus far, few studies have compared different types of physical exercise training protocols and their impact on BDNF concentrations, especially in participants over 60 years old. The main objective of this study was to compare the effects of three exercise protocols on plasma BDNF concentrations at rest in healthy older adults. Thirty-four older adults were randomized into three interventions: (1) lower body strength and aerobic training (LBS-A), (2) upper
Fig. 6 HSP105-siRNA in HT22 cells or stressed mouse brain decreased BDNF levels and abolished antidepressant effects.. (A) Level of HSP105 mRNA in HT22 cells (ANOVA, F2,13 = 544.1, n = 5 to 6). (B) Level of BDNF mRNA in HT22 cells (ANOVA, F2,13 = 10.74, n = 5 to 6). (C) The level of HSP105 protein in the hippocampus was detected by Western blotting (n = 3). (D) Immobility times in the forced swim test (ANOVA, F2,11 = 6.03). (E) Immobility times in the tail suspension test (ANOVA, F2,11 = 15.02). (F) Social interaction rate in the interaction test (ANOVA, F2,11 = 5.00). (G) Sucrose preference and total fluid intake in the sucrose preference test. (H) Level of BDNF mRNA and protein in the mouse hippocampus (ANOVA, F2,11 = 4.54 and F2,12 = 5.41, respectively) (n = 4 to 5 animals per group). Each bar indicates the mean ± SEM. GGA + NTC, GGA with nontargeting control; GGA + HSP105-siRNA, GGA with HSP105-siRNA treatment. Statistically different groups are indicated by letters. ...
Background: Brain-derived neurotrophic factor (BDNF) mutant mice show hyperphagia and hyperleptinemia. Animal and cell-culture experiments suggest multiple interrelations between BDNF and the serotonin (5-HT) system. We studied serum BDNF in patients with anorexia nervosa and its associations with peripheral indicators of the 5-HT system. To control for secondary effects of acute malnutrition, we assessed acutely underweight patients with anorexia nervosa (acAN) in comparison to long-term weight-recovered patients with the disorder (recAN) and healthy controls.. Methods: We determined serum BDNF, platelet 5-HT content and platelet 5-HT uptake in 33 patients in the acAN group, 20 patients in the recAN group and 33 controls. Plasma leptin served as an indicator of malnutrition.. Results: Patients in the acAN group were aged 14-29 years and had a mean body mass index (BMI) of 14.9 (standard deviation [SD] 1.4) kg/m2. Those in the recAN group were aged 15-29 years and had a mean BMI of 20.5 (SD 1.3) ...
Open peer review is a system where authors know who the reviewers are, and the reviewers know who the authors are. If the manuscript is accepted, the named reviewer reports are published alongside the article. Pre-publication versions of the article and author comments to reviewers are available by contacting [email protected] All previous versions of the manuscript and all author responses to the reviewers are also available.. You can find further information about the peer review system here.. ...
BDNF and VEGF were analyzed as continuous variables. VEGF values were log-transformed to normalize the skewed distribution of VEGF. We used Cox-proportional hazards models to relate baseline serum BDNF and logVEGF levels (separately) to risk of incident stroke/TIA in Study Sample 1. We first examined the linear effect of a 1-SD unit increase/decrease in BDNF and logVEGF on risk of stroke/TIA. We also explored threshold effects comparing the risk across quartiles of BDNF and VEGF. We observed a threshold effect with BDNF only. Therefore, we ran threshold models for BDNF using the lowest quartile, Q1, as the reference and also assessed a threshold model comparing risk for persons in Q1 with persons in Q2 to Q4. We performed a similar set of analyses on a Study Sample 1b with stroke alone as the outcome. Using multivariable linear and logistic regression models, we examined the cross-sectional associations between BDNF and logVEGF and markers of brain aging (WMHV, and VR-d and Trails B-A ...
TY - JOUR. T1 - Brain-derived neurotrophic factor promoter methylation and cortical thickness in recurrent major depressive disorder. AU - Na, Kyoung Sae. AU - Won, Eunsoo. AU - Kang, June. AU - Chang, Hun Soo. AU - Yoon, Ho-Kyoung. AU - Tae, Woo Suk. AU - Kim, Yong Ku. AU - Lee, Min-Soo. AU - Joe, Sook Haeng. AU - Kim, Hyun. AU - Ham, Byung-Joo. PY - 2016/2/15. Y1 - 2016/2/15. N2 - Recent studies have reported that methylation of the brain-derived neurotrophic factor (BDNF) gene promoter is associated with major depressive disorder (MDD). This study aimed to investigate the association between cortical thickness and methylation of BDNF promoters as well as serum BDNF levels in MDD. The participants consisted of 65 patients with recurrent MDD and 65 age-and gender-matched healthy controls. Methylation of BDNF promoters and cortical thickness were compared between the groups. The right medial orbitofrontal, right lingual, right lateral occipital, left lateral orbitofrontal, left pars ...
One of the heavy progressive vascular complications of type 2 diabetes is a central nervous system, manifesting cognitive dysfunction due to metabolic changes. Goal. Defining the role of brain-derived neurotrophic factor (BDNF) in the diagnosis of cognitive dysfunction in patients with type 2 diabetes. Materials and methods. The study involved 83 patients with type 2 diabetes at the age of 40 - 70 years. Complex examination included clinical and laboratory examination, neuropsychological testing. To screen for cognitive impairment used the Montreal Cognitive Assessment Scale (MOS test). To identify early markers of cognitive impairment was determined the level of brain-derived neurotrophic factor (BDNF). Results. The study found a negative correlation between the level of BDNF and the HbA1c (r = - 0,494, p = 0.01), fasting glucose (r = - 0,499, p = 0.01), and a positive relationship between the level of BDNF and cognitive function in patients with type 2 diabetes. Conclusion. In patients with ...
Background Following voxel-based morphometry (VBM), brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) has been shown to affect human brain morphology in Caucasians. However, little is known about the specific role of the Met/Met genotype on brain structure. Moreover, the relationship between BDNF Val66Met polymorphism and Chinese brain morphology has not been studied. Methodology/Principal Findings The present study investigated brain structural differences among three genotypes of BDNF (rs6265) for the first time in healthy young Chinese adults via cortical thickness analysis and VBM. Brain differences in Met carriers using another grouping method (combining Val/Met and Met/Met genotypes into a group of Met carriers as in most previous studies) were also investigated using VBM. Dual-approach analysis revealed less gray matter (GM) in the frontal, temporal, cingulate and insular cortices in the Met/Met group compared with the Val/Val group (corrected, P|0.05). Areas with less GM
Citation: Khundakar, A.A. and Zetterström, T.S.C. (2011) Effects of GABAB ligands alone and in combination with paroxetine on hippocampal BDNF gene expression. European Journal of Pharmacology, 671 (1-3) pp. 33-38 ...
A Val66Met single-nucleotide polymorphism (SNP) in the brain-derived neurotrophic factor (BDNF) gene impairs activity-dependent BDNF release in cultured hippocampal neurons and predicts impaired memory and exaggerated basal hippocampal activity in healthy humans. Several clinical genetic association studies along with multi-modal evidence for hippocampal dysfunction in schizophrenia indirectly suggest a relationship between schizophrenia and genetically determined BDNF function in the hippocampus. To directly test this hypothesized relationship, we studied 47 medication-free patients with schizophrenia or schizoaffective disorder and 74 healthy comparison individuals with genotyping for the Val66Met SNP and [15O]H2O positron emission tomography (PET) to measure resting and working memory-related hippocampal regional cerebral blood flow (rCBF). In patients, harboring a Met allele was associated with significantly less hippocampal rCBF. This finding was opposite to the genotype effect seen in healthy
The neurotrophin brain-derived neurotrophic factor (BDNF) plays a key role in synaptic plasticity, in part due to changes in local protein synthesis. Activation of TrkB (tropomyosin-related kinase B) receptors for BDNF triggers several parallel signaling pathways, including the Ras/ERK, the phosphatidylinositol 3-kinase (PI3-K) and the phospholipase C-γ pathways. Recent studies have elucidated some of the signaling mechanisms that contribute to the regulation of translation activity by BDNF, through modulation of initiation and elongation phases, but the resulting changes in the proteome are not yet fully characterized. The proteins synthesized in response to activation of TrkB receptors by BDNF depend on the mRNAs that are available locally, after delivery and transport along dendrites. Recent studies have shown that BDNF may also play a regulatory role at this level. Furthermore, BDNF regulates transcription activity, thereby affecting the array of mRNAs available to be transported along dendrites.
Brain-derived neurotrophic factor (BDNF) promotes several functions in neurons and modulates neurotransmissions, especially in hippocampal regions. Frontotemporal lobar degeneration (FTLD) has a strong genetic background, but genetic risk factors ass
Context: Brain-derived neurotrophic factor (BDNF) is a pleiotropic peptide also involved in maintaining endothelial integrity. It is unknown if circulating BDNF levels are associated with risk of cardiovascular disease (CVD).. Objective: To investigate the association of circulating BDNF with CVD risk Design, Setting and Participants: First, we prospectively investigated the association of circulating BDNF levels with cardiovascular events and mortality in the 3,687 participants (mean age 65 years, 2,068 women) from the Framingham Heart Study (FHS). Next, we evaluated the association of a common nonsynonymous SNP in the BDNF gene (rs6265) with circulating BDNF concentrations in FHS. Finally, we performed a Mendelian randomization experiment in the CARDIoGRAM consortium (,22,000 coronary artery disease [CAD] cases, ,60,000 controls) to investigate whether the same SNP was associated with CAD risk in CARDioGRAM and if so, whether the direction and effect size differed from that predicted based on ...
Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also appears to function downstream of the leptin-melanocortin signaling pathway to control appetite. In both animals and humans, diminished BDNF function is associated with hyperphagia, obesity, and neurocognitive deficits. We propose to study BDNF in two hyperphagic disorders: Prader-Willi syndrome and MC4R function-altering mutations. We hypothesize that patients with PWS may have increased BDNF during infancy, followed by a decline in BDNF that precedes the onset of hyperphagia and persists after the onset of obesity. We hypothesize that patients with MC4R mutations will have decreased BDNF, the severity of which will be associated with the degree of MC4R functional loss caused by the specific mutation(s) in each individual. To test these hypotheses, we wish to conduct cross-sectional studies to evaluate serum BDNF concentrations, metabolism, body composition, and ...
Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also appears to function downstream of the leptin-melanocortin signaling pathway to control appetite. In both animals and humans, diminished BDNF function is associated with hyperphagia, obesity, and neurocognitive deficits. We propose to study BDNF in two hyperphagic disorders: Prader-Willi syndrome and MC4R function-altering mutations. We hypothesize that patients with PWS may have increased BDNF during infancy, followed by a decline in BDNF that precedes the onset of hyperphagia and persists after the onset of obesity. We hypothesize that patients with MC4R mutations will have decreased BDNF, the severity of which will be associated with the degree of MC4R functional loss caused by the specific mutation(s) in each individual. To test these hypotheses, we wish to conduct cross-sectional studies to evaluate serum BDNF concentrations, metabolism, body composition, and ...
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Figure 4. Hippocampus and Perirhinal cortex in Human Brain (Figure Source). Some studies measured serum BDNF levels instead of specifically measuring brain BDNF concentration.[21][31][32][13] Serum BDNF is measured instead of brain levels because it can be measured without sacrificing the animal and is also acceptable for human studies. Acute changes in serum BDNF levels are thought to directly reflect changes in brain BDNF concentration[21][24]. There are several reasons for this: rat studies show correlations between serum and brain BDNF levels,[21] BDNF easily travels in both directions across the blood-brain barrier,[21][24] and both serum and brain BDNF levels are significantly reduced in AD.[24] There is conflicting evidence concerning exercise and its impact on serum BDNF.[24] Acute bouts of exercise have been found to increase serum BDNF levels,[21][24] but several studies have concluded that regular (chronic) exercise may lead to decreased serum BDNF levels compared to sedentary ...
The Effects of Voluntary, Involuntary, and Forced Exercises on Brain-Derived Neurotrophic Factor and Motor Function Recovery: A Rat Brain Ischemia Model - free full-text /PMC3035657/ - Feb 2011 I was happy to find that what I have personally experienced has been proven to be true: forced exercise is not as beneficial as voluntary. Sometimes science…
Environmental enrichment (EE) refers to the provision of a complex and stimulating housing condition which improves well-being, behaviour and brain function of laboratory animals. The mechanisms behind these beneficial effects of EE are only partially understood. In the current report, we describe a link between EE and neuropeptide Y (NPY), based on findings from NPY knockout (KO) mice exposed to EE. Relative to EE-housed wildtype (WT) animals, NPY KO mice displayed altered behaviour as well as molecular and morphological changes in amygdala and hippocampus. Exposure of WT mice to EE reduced anxiety and decreased central glucocorticoid receptor expression, effects which were absent in NPY KO mice. In addition, NPY deletion altered the preference of EE items, and EE-housed NPY KO mice responded to stress with exaggerated hyperthermia, displayed impaired spatial memory, had higher hippocampal brain-derived neurotrophic factor mRNA levels and altered hippocampal synaptic plasticity, effects which were not
Sigma-Aldrich offers abstracts and full-text articles by [Erica D Smith, G Aleph Prieto, Liqi Tong, Ilse Sears-Kraxberger, Jeffrey D Rice, Oswald Steward, Carl W Cotman].
The brain-derived neurotrophic factor (BDNF) is essential for the survival of neurons in the central nervous system (CNS). The expression of BDNF is regulated by several conditions related to neuronal activity including seizures, normal neuronal depolarization, and long-term potentiation (LTP)--all mechanisms that increase intracellular concentrations of calcium. Increased calcium leads to the occupation of calcium-adenosine-3′,5′-monophosphate (cAMP) response element (CRE) in the BDNF promoter by transcription factors of the CRE-binding protein (CREB) family. The BDNF gene contains four noncoding exons located 5′ to the coding region, each of which can be alternatively spliced to the 3′ coding exon. BDNF mRNAs that contain the nontranslated exon 3 are the most highly expressed isoform in response to membrane depolarization. In an attempt to understand the processes that contribute to activity-induced neuronal gene-expression, Tao et al. have identified a new mechanism by which BDNF ...
Brain-Derived Neurotrophic Factor: A member of the nerve growth factor family of trophic factors. In the brain BDNF has a trophic action on retinal, cholinergic, and dopaminergic neurons, and in the peripheral nervous system it acts on both motor and sensory neurons. (From Kendrew, The Encyclopedia of Molecular Biology, 1994)
Background: Brain-derived neurotrophic factor (BDNF) is associated with coronary artery diseases. However, its role and mechanism in myocardial infarction (MI) is not fully understood. Methods: ...
Human neural stem cells genetically modified to overexpress brain-derived neurotrophic factor promote functional recovery and neuroprotection in a mouse stroke model. - Hong J Lee, In J Lim, Min C Lee, Seung U Kim
The role of brain-derived neurotrophic factor in the regulation of cell growth and gene expression in melanotrope cells of Xenopus laevis Academic Article ...
Neurotrophic factors are critical regulators of the formation and plasticity of neuronal networks. Brain-derived neurotrophic factor (BDNF) is abundant in the brain and periphery, and is found in both human serum and plasma. Animal studies have demonstrated that stress reduces BDNF expression or activity in the hippocampus and that this reduction can be prevented by treatment with antidepressant drugs. A similar change in BDNF activity occurs in the brain of patients with major depression disorder (MDD). Recently, clinical studies have indicated that serum or plasma BDNF levels are decreased in untreated MDD patients. Antidepressant treatment for at least four weeks can restore the decreased BDNF function up to the normal value. Therefore, MDD is associated with impaired neuronal plasticity. Suicidal behavior can be a consequence of severe impaired neuronal plasticity in the brain. Antidepressant treatment promotes increased BDNF activity as well as several forms of neuronal plasticity, ...
Have you ever heard the term "runners high?" Is it really possible to feel that good, just from exercise? You bet it is. Exercise can activate the same pathways in the brain as morphine and increases the release of endorphins, natural feel-good neurotransmitters. That makes exercise the closest thing to a happiness pill you will ever find.. Boost your mood. Physical exercise stimulates neurotransmitter activity-specifically norepinephrine, dopamine, and serotonin-which elevates mood.. Fight depression. Exercise can be as effective as prescription medicine in treating depression. One of the reasons why exercise can be so useful is because it increases brain-derived neurotrophic factor (BDNF).. BDNF is like an anti-aging wonder drug that is involved with the growth of new brain cells. Think of BDNF as a sort of Miracle-Gro for your brain. BDNF not only grows new brain cells, but it is also instrumental in putting the brakes on depression.. The antidepressant benefits of exercise have been well ...
i] Ravindran P.N., Babu K.N., Sivaraman K. "Turmeric: The Genus Curcuma"; CRC Press Pg 5 March 1, 2007 ISBN 9780849370342 (source). [ii] "Tumeric" US National Library of Medicine ncbi.nlm.hih.gov Retrieved August 4, 2016 (source). [iii] "Turmeric" National Center for Complementary and Integrative Health nih.gov (source). [iv] Ng T.P., Chiam P.C., Lee T., Chua H.C., Lim L., Kua E.H. "Curry consumption and cognitive function in the elderly." American Journal of Epidemiology. 2006 Nov 1;164(9):898-906. (source). [v] Kulkarni S.K., Dhir A. "An Overview of Curcumin in Neurological Disorders" Indian Journal of Pharmaceutical Sciences. 2010 Mar-Apr; 72(2): 149-154. (source). [vi] Wang R., Li Y.B., Li Y.H., Xu Y., Wu H.L., Li X.J. "Curcumin protects against glutamate excitotoxicity in rat cerebral cortical neurons by increasing brain-derived neurotrophic factor level and activating TrkB."Brain Research. 2008 May 19;1210:84-91. (source). [vii] Kim S.J., Son T.G., Park H.R., Park M., Kim M.S., Kim H.S., ...
The proliferation, differentiation and survival of neuronal and glial cells are affected by a number of neurotrophic factors, such as nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and others. In a previous study, we observed the effects of `SEMAX® (Met-Glu-His-Phe-Pro-Gly-Pro), the physiologically active analogue of adrenocorticotropic hormone(4-10), on neuronal cell survival in vitro. We hypothesized that these effects may be mediated by the regulation of expression of some neurotrophic factors. To test this hypothesis we analyzed NGF and BDNF gene expression in glial cells obtained from the basal forebrain of newborn rats, following in vitro treatment with `SEMAX®. We observed changes in mRNA levels for both the NGF and BDNF genes. The greatest increase in expression was found after 30 min of `SEMAX® administration. At this time, BDNF mRNA level was increased eight-fold in comparison with control, and NGF mRNA level was increased five-fold. 2001 Elsevier Science ...
Our results demonstrate that genetic loss of MeCP2 is associated not only with deficits in neuronal BDNF content but also with a significant increase in the percentage of BDNF content available for release. Because deficits in BDNF protein levels are temporally regulated in a cell-type- or region-specific manner, the net effect of the Mecp2 −/y mutation on BDNF release will vary among neuronal populations and with age. The fact that newborn Mecp2 −/y neurons release abnormally high levels of BDNF raises the possibility that BDNF-dependent regulation of neural development is disrupted in mutant mice in vivo. For example, hypersecretion of BDNF, particularly by newborn Mecp2 −/y neurons at rest, could derange developmental processes that depend on tight coupling between neuronal activity and BDNF release, such as activity-dependent refinement of synaptic connections (Lein and Shatz, 2000). Additional studies are required to determine how the Mecp2 −/y mutation affects evoked release at ...
Executive function declines with age, but engaging in aerobic exercise may attenuate decline. One mechanism by which aerobic exercise may preserve executive function is through the up-regulation of brain-derived neurotropic factor (BDNF), which also declines with age. The present study examined BDNF as a mediator of the effects of a 1-year walking intervention on executive function in 90 older adults (mean age = 66.82). Participants were randomized to a stretching and toning control group or a moderate intensity walking intervention group. BDNF serum levels and performance on a task-switching paradigm were collected at baseline and follow-up. We found that age moderated the effect of intervention group on changes in BDNF levels, with those in the highest age quartile showing the greatest increase in BDNF after 1-year of moderate intensity walking exercise (p = .036). The mediation analyses revealed that BDNF mediated the effect of the intervention on task-switch accuracy, but did so as a function of
article{1fdd16d8-cade-46c6-b3bf-0719173f035c, abstract = {Both brain-derived neurotrophic factor (BDNF) and the serotonin receptor 2A (5-HT2A) have been related to depression pathology. Specific 5-HT2A receptor changes seen in BDNF conditional mutant mice suggest that BDNF regulates the 5-HT2A receptor level. Here we show a direct effect of BDNF on 5-HT2A receptor protein levels in primary hippocampal neuronal and mature hippocampal organotypic cultures exposed to different BDNF concentrations for either 1, 3, 5 or 7 days. In vivo effects of BDNF on hippocampal 5-HT2A receptor levels were further corroborated in (BDNF +/-) mice with reduced BDNF levels. In primary neuronal cultures, 7 days exposure to 25 and 50 ng/mL BDNF resulted in downregulation of 5-HT2A, but not of 5-HT1A, receptor protein levels. The BDNF-associated downregulation of 5-HT2A receptor levels was also observed in mature hippocampal organotypic cultures, excluding confounding effects of BDNF on immature tissue. BDNF +/- mice ...
Brain-derived neurotrophic factor (BDNF) is a key player in synaptic plasticity, and consequently, learning and memory. Because of its fundamental role in numerous neurological functions in the central nervous system, BDNF has utility as a biomarker and drug target for neurodegenerative and neuropsychiatric disorders. Here, we generated a screening assay to mine inducers of Bdnf transcription in neuronal cells, using primary cultures of cortical cells prepared from a transgenic mouse strain, specifically, Bdnf-Luciferase transgenic (Bdnf-Luc) mice. We identified several active extracts from a library consisting of 120 herbal extracts. In particular, we focused on an active extract prepared from Ginseng Radix (GIN), and found that GIN activated endogenous Bdnf expression via cAMP-response element-binding protein-dependent transcription. Taken together, our current screening assay can be used for validating herbal extracts, food-derived agents, and chemical compounds for their ability to induce Bdnf
BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF). BDNF is the dominant factor (compared to other neurotrophic factors) in the brain. This holds true not only to the variety of brain structures, but also to the BDNF expression level. According to our data [16, 17], BDNF expression in the brain structures of rats is much higher than that of GDNF. According to current estimations, the human BDNF gene is located in the p14 region of chromosome 11 (in rats and mice these are chromosomes 3q33 and 2qE3, respectively) and contains 12 exons, nine of which have specific promoters (I-VIII 5′ exons spliced to the common 3′ IX exon). This gene structure is observed both in humans [18] and in rodents [19], but the number of exons varies (9 in mice and 10 in rats). Transcripts of template RNA as well as BDNF protein are widely present in the neocortex, hippocampus, amygdala, and cerebellum [20].. BDNF is notable by structural and functional complexity, which is based on (i) the presence of several promoters in the ...
The response of embryonic chick nodose ganglion (neural placode-derived) and dorsal root ganglion (neural crest-derived) sensory neurons to the survival and neurite-promoting activity of brain-derived neurotrophic factor (BDNF) was studied in culture. In dissociated, neuron-enriched cultures established from chick embryos between Day 6 (E6) and Day 12 (E12) of development, both nodose ganglion (NG) and dorsal root ganglion (DRG) neurons were responsive on laminin-coated culture dishes to BDNF. In the case of NG, BDNF elicited neurite outgrowth from 40 to 50% of the neurons plated at three embryonic ages; E6, E9, and E12. At the same ages, nerve growth factor (NGF) alone or in combination with BDNF, had little or no effect upon neurite outgrowth from NG neurons. The response of NG neurons to BDNF was dose dependent and was sustainable for at least 7 days in culture. Surprisingly, in view of a previous study carried out using polyornithine as a substrate for neuronal cell attachment, on ...
BDNF antibody (brain-derived neurotrophic factor) for ELISA. Anti-BDNF pAb (GTX17884) is tested in Human, Mouse samples. 100% Ab-Assurance.
OBJECTIVE: To evaluate whether an animal model of mania induced by lisdexamfetamine dimesylate (LDX) has an inflammatory profile and whether immune activation by lipopolysaccharides (LPS) has a cumulative effect on subsequent stimuli in this model. We also evaluated the action of lithium (Li) on inflammatory and neurotrophic factors. METHODS: Adult male Wistar rats were subjected to an animal model of mania. After the open-field test, they were given LPS to induce systemic immune activation. Subsequently, the animals blood was collected, and their serum levels of brain-derived neurotrophic factor and inflammatory markers (tumor necrosis factor [TNF]-α, interleukin [IL]-6, IL-1β, IL-10, and inducible nitric oxide synthase [iNOS]) were measured. RESULTS: LDX induced hyperactivity in the animals, but no inflammatory marker levels increased except brain-derived neurotrophic factor (BDNF). Li had no effect on serum BDNF levels but prevented iNOS levels from increasing in animals subjected to immune
Several studies have recently reported that chromatin-modifying mechanisms are involved in learning and memory processes in adult neurons.3,5,35 For example, Levenson et al.35 showed that whereas histone H3 was acetylated following contextual FC in the hippocampus, histone H4 was acetylated following a latent inhibition protocol for contextual FC. Lubin et al.3 investigated histone modifications at specific BDNF promoters after contextual FC. They observed a selective increase in histone H3 acetylation at the BDNF gene promoter of exon IV, and a selective decrease in histone H4 acetylation at the BDNF promoter of exon II. In our study, SPS rats demonstrated a significant increase relative to sham rats in the levels of acetylated H3 and H4 at BDNF promoters of exons I and IV after FC. In addition, this selective increase in histone acetylation at the promoters of exons I and IV were consistent with up-regulation in exon I and IV mRNA transcription associated with FC. Interestingly, there were no ...
OBJECTIVE: Cross-sectional genetic association studies have reported equivocal results on the relationship between the brain-derived neurotrophic factor (BDNF) Val66Met and risk of Alzheimers disease (AD). As AD is a neurodegenerative disease, genetic influences may become clearer from prospective study. We aimed to determine whether BDNF Val66Met polymorphism influences changes in memory performance, hippocampal volume, and Aβ accumulation in adults with amnestic mild cognitive impairment (aMCI) and high Aβ. METHODS: Thirty-four adults with aMCI were recruited from the Australian, Imaging, Biomarkers and Lifestyle (AIBL) Study. Participants underwent PiB-PET and structural MRI neuroimaging, neuropsychological assessments and BDNF genotyping at baseline, 18 month, and 36 month assessments. RESULTS: In individuals with aMCI and high Aβ, Met carriers showed significant and large decline in episodic memory (d = 0.90, p = .020) and hippocampal volume (d = 0.98, p = .035). BDNF Val66Met was ...
... content are included within this article. axis prior to intracisternal infection with live meningitis, Brain-derived neurotrophic factor, Neuroinflammation, Hippocampal apoptosis Background Bacterial meningitis is a severe infection of the central nervous systems (CNS), with an annual occurrence of 0.9 per 100,000 Dasatinib biological activity people in developing countries [1, 2]. The most common causative agent is meningitis. Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophic family, which plays an important role in the development, differentiation, and survival of neurons in the CNS [11, 12]. BDNF exerts neuroprotective effects in multiple CNS diseases following its high-affinity binding to tropomyosin-receptor kinase B (TrkB) [13, 14]. In recent years, significant effort has been expended to identify the neuroprotective effects of BDNF on meningitis in both animal experiments and ...
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PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
Bioaim Human BDNF EasyTest™ ELISA Kit suitable for Plasma, Serum in human. Reliably quantify 1pg/ml of BDNF. It takes 1.5 hours.
UNLABELLED: Brain-derived neurotrophic factor (BDNF) is essential for neuronal differentiation and survival. We know that BDNF levels decline in the brains of patients with Huntingtons disease (HD), a neurodegenerative disease caused by the expression of mutant huntingtin protein (mHtt), and furthermore that administration of BDNF in HD mice is protective against HD neuropathology. BDNF is produced in neurons, but astrocytes are also an important source of BDNF in the brain. Nonetheless, whether mHtt affects astrocytic BDNF in the HD brain remains unknown. Here we investigated astrocytes from HD140Q knock-in mice and uncovered evidence that mHtt decreases BDNF secretion from astrocytes, which is mediated by exocytosis in astrocytes. Our results demonstrate that mHtt associates with Rab3a, a small GTPase localized on membranes of dense-core vesicles, and prevents GTP-Rab3a from binding to Rab3-GAP1, disrupting the conversion of GTP-Rab3a into GDP-Rab3a and thus impairing the docking of BDNF ...
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Previous research has found that adolescent ethanol (EtOH) exposure alters drug seeking behaviors, cognition and neuroplasticity. Using male Sprague Dawley rats, differences in spatial working memory, non-spatial discrimination learning and behavioral flexibility were explored as a function of age at the onset (mid-adolescent vs. adult) of chronic EtOH exposure (CET). Concentrations of mature brain-derived neurotrophic factor (mBDNF) and betanerve growth factor (beta-NGF) in the prefrontal cortex and hippocampus were also assessed at different time-points: during CET, following acute abstinence (48-hrs), and after protracted abstinence (6-8 wks). Our results revealed that an adolescent onset of CET leads to increased EtOH consumption that persisted into adulthood. In both adult and adolescent onset CET groups, there were significant long-term reductions in prefrontal cortical mBDNF and beta-NGF levels. However, only adult onset CET rats displayed decreased hippocampal BDNF levels. Spatial memory,
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Culture of cerebellar granule cells. Primary cultures of cerebellar granule cells were prepared from 8-d-old (P8) ICR mice (Japan SLC, Hamamatsu, Japan) according to the procedures described byFischer (1982) with minor modifications. Briefly, cerebella from P8 mice were treated with 0.1% trypsin and 0.05% DNase I in Ca2+/Mg2+-free HBSS at 37°C for 15 min and tritiated by pipetting in DNase I containing Ca2+-free HBSS. Dissociated cells were suspended in growth medium composed of basal medium Eagle (Sigma, St. Louis, MO) supplemented with 5% horse serum, 100 U/ml penicillin, and 0.1 mg/ml streptomycin (all from Life Technologies, Rockville, MD), 1 mg/ml bovine serum albumin (BSA), 10 μg/ml insulin, 0.1 nml-thyroxine, 0.1 mg/ml transferrin, 1 μg/ml aprotinin, 30 nm selenium, 0.25% glucose, and 2 mg/ml sodium bicarbonate (all from Sigma). Cells were plated at a density of 2 × 105cells/cm2 onto poly-d-lysine-coated 100 mm culture dishes (Becton Dickinson, Franklin Lakes, NJ). On the following ...
PRF readers can get free access to a selected Journal of Pain paper each month, thanks to the American Pain Society. Get the free full text of the selection from the February 2018 issue here.. ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
International Journal of Endocrinology is a peer-reviewed, Open Access journal that provides a forum for scientists and clinicians working in basic and translational research. The journal publishes original research articles, review articles, and clinical studies that provide insights into the endocrine system and its associated diseases at a genomic, molecular, biochemical and cellular level.
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By mopping up excess neurotrophic factor from neuronal synapses, astrocytes may finely tune synaptic transmission to affect processes such as learning and memory, say Bergami et al.. The major cellular events of learning and memory are long-term potentiation (LTP) and long-term depression (LTD), both of which affect neurons ability to communicate with one another. Neurons that have undergone LTP display a stronger electrical response to the same level of a stimulus, whereas neurons that have gone through LTD display a weaker response. These changes are thought to result from modifications of the neuronal synapses, such as alterations in the density of postsynaptic receptors, or downstream signaling events.. Secretion of the neurotrophic factor BDNF (brain-derived neurotrophic factor) has been implicated in long-term synaptic modification, and the function of BDNF on synaptic strength depends on its particular form: in its pro-BDNF form it is believed to promote LTD, and in its mature form it ...
TY - JOUR. T1 - Multiple functions of precursor BDNF to CNS neurons. T2 - Negative regulation of neurite growth, spine formation and cell survival. AU - Koshimizu, Hisatsugu. AU - Kiyosue, Kazuyuki. AU - Hara, Tomoko. AU - Hazama, Shunsuke. AU - Suzuki, Shingo. AU - Uegaki, Koichi. AU - Nagappan, Guhan. AU - Zaitsev, Eugene. AU - Hirokawa, Takatsugu. AU - Tatsu, Yoshiro. AU - Ogura, Akihiko. AU - Lu, Bai. AU - Kojima, Masami. PY - 2009/9/24. Y1 - 2009/9/24. N2 - Background. Proneurotrophins and mature neurotrophins elicit opposite effects via the p75 neurotrophin receptor (p75NTR) and Trk tyrosine kinase receptors, respectively; however the molecular roles of proneurotrophins in the CNS are not fully understood. Results. Based on two rare single nucleotide polymorphisms (SNPs) of the human brain-derived neurotrophic factor (BDNF) gene, we generated R125M-, R127L- and R125M/R127L-BDNF, which have amino acid substitution(s) near the cleavage site between the pro- and mature-domain of BDNF. Western ...
Brain-derived neurotrophic factor (BDNF) is involved in multiple aspects of synaptogenesis, from the formation to the functional maturation of synapses. BDNF influences the morphological complexity of axons and dendrites [15-17], increases synapse number [18-20], modulate synaptic maturation and controls ultrastructural composition of synapses [21, 22]. BDNF is critical for synaptic plasticity and memory processing in adult brain and is also essential to promote short and long term memory [23-26]. BDNF is synthesized as a precursor (pro-BDNF) encompassing two domains, the prodomain and the mature BDNF domain [27]. The pro-BDNF is cleaved by prohormone convertases such as furin and PC1/3 intracellularly or plasminogen/plasmin and MMPs extracellularly [28-30] to release the mature form [31].. Our data show that ApoE2 induces the astrocytes to secrete more m-BDNF than does ApoE3, while ApoE4 produces a negligible amount. We also found that the secreted pro-BDNF level was higher in ApoE3-treated ...
Running rodents make more of a "Miracle-Gro" chemical for the brain. A protein called brain-derived neurotrophic factor, or BDNF, has been labeled as the "Miracle-Gro" protein in the brain based on its role in enhancing memory and the growth of nerve cells. Researchers found in a study using mice that BDNF levels increase within the brain when the mice exercise on the wheel. "We believe that our study shows a precise biological mechanism behind increased BDNF production in mammals due to exercise," says study senior investigator and cell biologist Moses Chao, PhD. "Unraveling the mysteries of BDNF is important as we seek more ways to naturally keep mammalian brains healthy, including those or people," said Chao, a professor at NYU Langone and its Skirball Institute of Biomolecular Medicine. To read more, click here.. ...
Septic patients frequently develop cognitive impairment that persists beyond hospital discharge. The impact of sepsis on electrophysiological and molecular determinants of learning is underexplored. We observed that mice that survived sepsis or endotoxemia experienced loss of hippocampal long-term potentiation (LTP), a brain-derived neurotrophic factor-mediated (BDNF-mediated) process responsible for spatial memory formation. Memory impairment occurred despite preserved hippocampal BDNF content and could be reversed by stimulation of BDNF signaling, suggesting the presence of a local BDNF inhibitor. Sepsis is associated with degradation of the endothelial glycocalyx, releasing heparan sulfate fragments (of sufficient size and sulfation to bind BDNF) into the circulation. Heparan sulfate fragments penetrated the hippocampal blood-brain barrier during sepsis and inhibited BDNF-mediated LTP. Glycoarray approaches demonstrated that the avidity of heparan sulfate for BDNF increased with sulfation at ...
Septic patients frequently develop cognitive impairment that persists beyond hospital discharge. The impact of sepsis on electrophysiological and molecular determinants of learning is underexplored. We observed that mice that survived sepsis or endotoxemia experienced loss of hippocampal long-term potentiation (LTP), a brain-derived neurotrophic factor-mediated (BDNF-mediated) process responsible for spatial memory formation. Memory impairment occurred despite preserved hippocampal BDNF content and could be reversed by stimulation of BDNF signaling, suggesting the presence of a local BDNF inhibitor. Sepsis is associated with degradation of the endothelial glycocalyx, releasing heparan sulfate fragments (of sufficient size and sulfation to bind BDNF) into the circulation. Heparan sulfate fragments penetrated the hippocampal blood-brain barrier during sepsis and inhibited BDNF-mediated LTP. Glycoarray approaches demonstrated that the avidity of heparan sulfate for BDNF increased with sulfation at ...
Neurodegenerative diseases represent a major public health problem, but beneficial clinical treatment with neurotrophic factors has not been established yet. The therapeutic use of neurotrophins has been restrained by their instability and rapid degradation in biological medium. A variety of strategies has been proposed for the administration of these leading therapeutic candidates, which are essential for the development, survival and function of human neurons. In this review, we describe the existing approaches for delivery of brain-derived neurotrophic factor (BDNF), which is the most abundant neurotrophin in the mammalian central nervous system (CNS). Biomimetic peptides of BDNF have emerged as a promising therapy against neurodegenerative disorders. Polymer-based carriers have provided sustained neurotrophin delivery, whereas lipid-based particles have contributed also to potentiation of the BDNF action. Nanotechnology offers new possibilities for the design of vehicles for neuroprotection and
Bodyweight and food intake are regulated by the hypothalamus which integrates peripheral hormonal and neural signals. The G-protein-coupled melanocortin-receptors 3 and 4 (MC3R and MC4R) are activated by melanocortins or inhibited by agouti-related pepetide (AgRP) and signal via the cAMP pathway. Brain-derived neurotrophic Factor (BDNF) was recently shown to signal downstream the MC4R via its receptor TrkB (tropomyosin-related kinase). Mutations in the MC4R are the most common cause of monogenetic obesity. However, many of these mutations are not functionally relevant in vitro. Here, an amino acid alignment of orthologous MC4R from over 70 species was used to evaluate reported mutations. Loss-of-function mutations were predominantly located at highly conserved positions whereas mutations without effect were located at non-conserved positions. Functional characterization of MC4R point mutations I194F (partial loss of function) and Y302C (complete loss of function) identified in mouse models ...
... long-term forms of synaptic plasticity and memory formation, but the mechanisms controlling Arc protein function are little known. LTP consolidation requires a period of sustained Arc synthesis driven by brain-derived neurotrophic factor (BDNF) signaling. Local infusion of the BDNF scavenger, TrkB-Fc, during LTP maintenance resulted in rapid reversion of LTP, inhibition of Arc synthesis and loss of enhanced Arc SUMO1ylation. Furthermore, coimmunoprecipitation analysis showed that SUMO1-ylated Arc forms a complex with the F-actin-binding protein drebrin A, a major regulator of cytoskeletal dynamics in dendritic spines. Although MPSL1 Arc also interacted with dynamin 2, calcium/calmodulindependentprotein kinase II-beta (CaMKII), and postsynaptic density protein-95 (PSD-95), these complexes lacked SUMOylated Arc. The results support a model in which newly synthesized Arc is SUMOylated and targeted ...
Herein we present a concept in cancer where an immune response is detrimental rather than helpful. In the cancer setting, the immune system is generally considered to be helpful in curtailing the initiation and progression of tumors. In this work we show that a patients immune response to their tumor can, in fact, either enhance or inhibit tumor cell growth. Two closely related autoantibodies to the growth factor receptor TrkB were isolated from cancer patients B cells. Although highly similar in sequence, one antibody was an agonist while the other was an antagonist. The agonist antibody was shown to increase breast cancer cell growth both in vitro and in vivo, whereas the antagonist antibody inhibited growth. From a mechanistic point of view, we showed that binding of the agonist antibody to the TrkB receptor was functional in that it initiated downstream signaling identical to its natural growth factor ligand, brain-derived neurotrophic factor (BDNF). Our study shows that individual ...
The brain-derived neurotrophic factor (BDNF) interacts with important genetic Alzheimers disease (AD) risk factors. Specifically, variants within the SORL1 gene determine BDNFs ability to reduce amyloid β (Aβ) in vitro. We sought to test whether functional BDNF variation interacts with SORL1 genotypes to influence expression and downstream AD-related processes in humans. Read & Research Alzheimers More. ...
of knowledge concerning its neurochemical aspects. There is increasing evidence that brain-derived neurotrophic factor (BDNF) and Nerve growth factor (NGF) are involved in the pathophysiology and treatment of depression through binding and activating their cognate receptors trk B and trk A respectively. The present study was performed to examine whether the expression profiles of BDNF and/or trk B as well as NGF and/or trk A were altered in postmortem brain in subjects who ...
Aging Nervous System. Neurotrophic Factors Necessary for Maintenance of Neurons. Nerve growth factor Brain-derived neurotrophic factor (BDNF) Neurotrophin 3 (NT3) Neurotrophin 4/5 (NT4,5). Neurotrophin function Play role in development of NS Slideshow 4289936 by elden
Specifically, CEP-1347 increases BDNF mRNA levels in the imagination compared to agency, which correlates with a reduction of disease spread in R6/2 mice, an experimental model of HD (Apostol et al. Using animal models, researchers be dressed shown that evoked seizures or epilepsy many times acti- vates the anyhow signalling pathways, and drugs or genetic modulation of these cas- cades can compress sense injury. even for those powerless by symptom 25 mg viagra super active with mastercard impotence or ed. In the surroundings of the vaccination-induced reduc- tion in the practice of HPV 16 and 18 infections interconnected to other oncogenic types, cytology could potentially suit less sensitive as regards detecting high-grade CIN. If there is remaining dishwater in the formulation, then the amount weighed want be inaccurate and this determination wear the guess of anaesthetize loading, which is expressed as mg psychedelic per mg particles. Sutherland, A M, K R Walley, and J A author 2005a generic ...
When you start exercising, your heart beat increases and so does your breathing. Your brain identifies this moment as "stress", or the so called "Fight or Flight" state. Your body believes you are in stress and will give you the energy you need to either "fight your enemy" or "fly away" from the source of stress. The protein BDNF (Brain-Derived Neurotrophic Factor) is then released. BDNF acts as a protector from stress, repairs memory neurons and acts as a reset button. Wonder now why you feel like you get a second start of the day after dancing or exercising? This is why after exercising your ideas will feel clearer and you will feel at ease. ...
BDNF - BDNF (untagged)-Human brain-derived neurotrophic factor (BDNF), transcript variant 1 available for purchase from OriGene - Your Gene Company.
Receptor tyrosine kinase involved in the development and the maturation of the central and the peripheral nervous systems through regulation of neuron survival, proliferation, migration, differentiation, and synapse formation and plasticity. Receptor for BDNF/brain-derived neurotrophic factor and NTF4/neurotrophin-4. Alternatively can also bind NTF3/neurotrophin-3 which is less efficient in activating the receptor but regulates neuron survival through NTRK2. Upon ligand-binding, undergoes homodimerization, autophosphorylation and activation. Recruits, phosphorylates and/or activates several downstream effectors including SHC1, FRS2, SH2B1, SH2B2 and PLCG1 that regulate distinct overlapping signaling cascades. Through SHC1, FRS2, SH2B1, SH2B2 activates the GRB2-Ras-MAPK cascade that regulates for instance neuronal differentiation including neurite outgrowth. Through the same effectors controls the Ras-PI3 kinase-AKT1 signaling cascade that mainly regulates growth and survival. Through PLCG1 and ...
Nerve growth factor (NGF) is known to play a key role in the development of hyperalgesia after inflammatory injury. The increased levels of NGF that accompany injury lead to hyperalgesia via peripheral and central spinal mechanisms. New evidence reviewed here indicates that NGF can directly sensitize nociceptive neurones to noxious heat stimuli through rapid modulation of heat/vanilloid receptors or via de-novo increased expression of heat receptors. In addition, new data suggest that the central sensitization that can result from increased NGF may be mediated via central release of another neurotrophin, brain-derived neurotrophic factor ...
Astrocytes (GFAP) in the dentate gyrus of a mouse hippocampus. Image courtesy of Dr. Ahmad Salehi, Stanford University. It is well known that physical exercise eases the symptoms of neurodegenerative disorders like Alzheimers disease and helps to prevent their onset. Researchers at Stanford University are working on figuring out how it happens.. In their study, published in the journal Brain Structure and Function, scientists in Dr. Ahmad Salehis lab examined the effects of physical exercise on astrocytes in a region of the mouse brain that is critical for cognition - the dentate gyrus of the hippocampus. Previous studies have shown that an increase in the expression of brain-derived neurotrophic factor (Bdnf) occurs in this region after exercise (Philips, Salehi et al 2014). Bdnf is a protein that supports the survival of existing neurons and encourages new growth, playing an important role in cognitive function.. While the current study reconfirms that exercise generates increased levels of ...
Astrocytes (GFAP) in the dentate gyrus of a mouse hippocampus. Image courtesy of Dr. Ahmad Salehi, Stanford University. It is well known that physical exercise eases the symptoms of neurodegenerative disorders like Alzheimers disease and helps to prevent their onset. Researchers at Stanford University are working on figuring out how it happens.. In their study, published in the journal Brain Structure and Function, scientists in Dr. Ahmad Salehis lab examined the effects of physical exercise on astrocytes in a region of the mouse brain that is critical for cognition - the dentate gyrus of the hippocampus. Previous studies have shown that an increase in the expression of brain-derived neurotrophic factor (Bdnf) occurs in this region after exercise (Philips, Salehi et al 2014). Bdnf is a protein that supports the survival of existing neurons and encourages new growth, playing an important role in cognitive function.. While the current study reconfirms that exercise generates increased levels of ...
The treatment reversed the process of dendritic retraction in the brains of rats.. Previous rat research has established that a substance referred to as ampakine can improve age-related cognitive deficits, which can boost manufacture of a vital growth factor, brain-derived neurotrophic factor (BDNF).. Rodent, monkey and scientific testing on people have established that dendrites decline with time, beginning in mid-life. The operation is known as dendritic retraction. Dendrites would be the branch-like fibers that stretch from neurons and receive signals using their company neurons.. Researchers in the College of California-Irvine desired to know whether dendritic retraction had been occurring in 13-month-old - or "middle-aged" - rats and, if thats the case, whether ampakine could reverse it.. They placed 10-month-old male rats in cages with enriched environments and gave them lots of space, a sizable running wheel and objects to understand more about. Every single day for several several ...
Tufts University, Health Sciences Campus. A protein directs appetite suppressor in the brain; implications for obesity treatment. A new neuroscience study sheds light on the biological underpinnings of obesity. The in vivo study, published in the January 8 issue of the Journal of Neuroscience, reveals how a protein in the brain helps regulate food intake and body weight. The findings reveal a potential new avenue for the treatment of obesity and may help explain why medications that are prescribed for epilepsy and other conditions that interfere with this protein, such as gabapentin and pregabalin, can cause weight gain.. The protein - alpha2/delta-1 - has not been linked previously to obesity. A team led by Maribel Rios, Ph.D., associate professor in the department of neuroscience at Tufts University School of Medicine, discovered that alpha2/delta-1 facilitates the function of another protein called brain-derived neurotrophic factor (BDNF). A previous study by Rios determined that BDNF plays a ...
Exercise the release of brain-derived neurotrophic factor (BDNF). Exercise causes a beneficial response in the brain and an increase of BDFN, which is a trophic factor which is linked to cognitive improvement and the alleviation of anxiety and depression. The levels of this protein have been found to increase after exercise. You may already have experienced this before when in an anxious state. Exercise seems to alleviate the anxiety and make you have clearer thoughts. As you get older, your mental sharpness decreases slowly. You can delay this through regular exercise from a young age.. As you get older, maintaining a healthy weight or losing weight becomes even more difficult. Given that most people tend to go into a sedentary lifestyle as they age, it may seem almost impossible. Your metabolism also slows down, meaning that you burn fewer calories. The best remedy for this is maintaining a consistent workout schedule consisting of strength and cardio workouts at least 3 times a week. This ill ...
Background and Purpose-Prophylactic treatments that afford neuroprotection against stroke may emerge from the field of preconditioning. Resveratrol mimics ischemic preconditioning, reducing ischemic brain injury when administered 2 days before global ischemia in rats. This protection is linked to silent information regulator 2 homologue 1 (Sirt1) and enhanced mitochondrial function possibly through its repression of uncoupling protein 2. Brain-derived neurotrophic factor (BDNF) is another neuroprotective protein associated with Sirt1. In this study, we sought to identify the conditions of resveratrol preconditioning (RPC) that most robustly induce neuroprotection against focal ischemia in mice. ...
Exercise the release of brain-derived neurotrophic factor (BDNF). Exercise causes a beneficial response in the brain and an increase of BDFN, which is a trophic factor which is linked to cognitive improvement and the alleviation of anxiety and depression. The levels of this protein have been found to increase after exercise. You may already have experienced this before when in an anxious state. Exercise seems to alleviate the anxiety and make you have clearer thoughts. As you get older, your mental sharpness decreases slowly. You can delay this through regular exercise from a young age.. As you get older, maintaining a healthy weight or losing weight becomes even more difficult. Given that most people tend to go into a sedentary lifestyle as they age, it may seem almost impossible. Your metabolism also slows down, meaning that you burn fewer calories. The best remedy for this is maintaining a consistent workout schedule consisting of strength and cardio workouts at least 3 times a week. This ill ...
The Baoji Xu laboratory researches the mechanisms by which growth factors such as brain-derived neurotrophic factor (BDNF) regulate the development and function of brain neural circuits that control learning, mood, appetite, energy expenditure, and body weight
Mowla SJ, Pareek S, Farhadi HF, Petrecca K, Fawcett JP, Seidah NG, Morris SJ, Sossin WS, Murphy RA. Differential sorting of nerve growth factor and brain-derived neurotrophic factor in hippocampal neurons ...
Affiliation:国際医療福祉大学,臨床医学研究センター,医師, Research Field:Cerebral neurosurgery,Nerve anatomy/Neuropathology, Keywords:ラット,神経分化,nerve growth factor,brain-derived neurotrophic factor,neuronal differentiation,細胞分裂,アドリアマイシン,アントラサイクリン,ニワトリ,gene transfer, # of Research Projects:4, # of Research Products:0
Exercise is centrally located in the wellness pyramid because it does it all. The endorphins will help with Contentment; the antioxidant defense system will help with Brain Maintenance; the brain-derived neurotrophic factor will help with Brain Enhancement. Exercise alone will not achieve any of the above; Ive covered other things to consider for Contentment and Brain Maintenance; let us now explore what else works to enhance the brain.. Brain enhancement refers to activities that stimulate the neurotransmitters of the brain to wire or rewire. Dexterity is one such activity. Indeed, an early test for cognitive decline is whether you can balance on one foot for twenty seconds. Do not try this every day, for you eventually will succeed simply through a form of rote learning, but every year or so you might want to see what happens.. The best dexterity for brain health is finger dexterity. All the parts involved in precisely moving your fingers call for greater brain power than any other activity, ...
Since weight training doesnt cause the same spike, few researchers have thought that it would have a similar effect. But recent studies intimate otherwise. Several studies involve animals. Its not easy, of course, to induce a mouse or a lab rat to lift weights, so the experimenters have to develop clever approximations of resistance training to see what impact adding muscle and strength has on an animals brain. In a study presented at the annual meeting of the Society for Neuroscience in November, researchers from Brazil secured weights to the tails of a group of rats and had them climb a ladder five sessions a week. Other rats on the same schedule ran on a treadmill, and a third group just sat around. After eight weeks, the running rats had much higher levels of brain-derived neurotrophic factor (B.D.N.F.), a growth factor that is thought to help spark neurogenesis, than the sedentary rats. So did the rats with weights tied to their tails. The weight--bearing rats, like the runners, did well ...
Higher level of protein from the gene called brain-derived neurotrophic factor may provide a buffer for the brain and protect it against the effects of the plaques.
Human BDNF (Brain Derived Neurotrophic Factor) ELISA Kit assay has a sensitivity of |2pg/ml. Measure BDNF (Brain Derived Neurotrophic Factor) in serum, blood, plasma, cell supernatant samples.
Neurotrophic factors (NTFs) are molecules which act to promote the differentiation of neurons and to maintain their phenotype. The discovery by Hamburger and Levi- Montalcini in 1949 that the number...
2 reviews. Compare Brain Derived Neurotrophic Factor ELISA Kits from leading suppliers on Biocompare. View specifications, prices, citations, reviews, and more.
Besides the induction of acute neurotrophin effects through intracellular signaling cascades within seconds to minutes (11, 43, 44, 47), a much faster and distinctly different excitatory action of neurotrophins has been reported. BDNF and NT-4/5, when applied locally and transiently to various types of central neurons, depolarize neurons within milliseconds, resulting in trains of action potentials (29). Intriguingly, application of only 6.43 nM (175 ng/ml) exogenous BDNF to CA1 pyramidal neurons elicits a response comparable with application of 25 μM glutamate. Thus the neurotrophins BDNF and NT-4/5 are effective at much lower concentrations than glutamate (29). The study cited also revealed that the rapid neurotrophin-evoked depolarization results from the immediate activation of a Na+ conductance. The Na+ conductance (BDNF-evoked INa) is insensitive to tetrodotoxin, a highly potent blocker of those voltage-gated Na+ channels that are involved in action potential firing (13).. Molecular ...
The involvement of neurotrophic factors in neuronal survival and differentiation is well established. The more recent realization that these factors also play pivotal roles in the maintenance and...
Keywords: SKF 83959 brain-derived neurotrophic aspect tropomyosin receptor kinase B juvenile prefrontal cortex nucleus accumbens Launch Adolescence is an interval of maturation in the corticolimbic parts of the mind and proof shows that this stage of advancement may coincide with the original manifestation of symptoms connected with neuropsychiatric disease. Symptoms of despair and schizophrenia for instance show significant boosts during adolescence [1 2 a developmental period also connected with elevated awareness to psychostimulant-induced praise [3-6]. Brain-derived neurotrophic aspect (BDNF) an associate from the neurotrophin category of development factors MLN518 acts inside the central anxious program via the tropomyosin receptor kinase B (TrkB) to aid the success of existing neurons [7 8 maintain neuronal synapse integrity [9] and promote neuronal development and differentiation [8 10 Because of these important activities on neuronal plasticity BDNF continues to be postulated to become ...
J Neuroinflammation. 2017 Aug 4;14(1):156. doi: 10.1186/s12974-017-0930-6.. Brain-derived neurotrophic factor reduces inflammation and hippocampal apoptosis in experimental Streptococcus pneumoniae meningitis.. Xu D1, Lian D1, Wu J1, Liu Y2, Zhu M3, Sun J3, He D1, Li L4.. Author information. Abstract. BACKGROUND:. Streptococcus pneumoniae meningitis is a serious inflammatory disease of the central nervous system (CNS) and is associated with high morbidity and mortality rates. The inflammatory processes initiated by recognition of bacterial components contribute to apoptosis in the hippocampal dentate gyrus. Brain-derived neurotrophic factor (BDNF) has long been recommended for the treatment of CNS diseases due to its powerful neuro-survival properties, as well as its recently reported anti-inflammatory and anti-apoptotic effects in vitro and in vivo.. METHODS:. In this study, we investigated the effects of BDNF-related signaling on the inflammatory response and hippocampal apoptosis in ...
Brain-derived neurotrophic factor (BDNF) promotes the biochemical and morphological differentiation of selective populations of neurons during development. In this study we examined the energy requirements associated with the effects of BDNF on neuronal differentiation. Because glucose is the preferred energy substrate in the brain, the effect of BDNF on glucose utilization was investigated in developing cortical neurons via biochemical and imaging studies. Results revealed that BDNF increases glucose utilization and the expression of the neuronal glucose transporter GLUT3. Stimulation of glucose utilization by BDNF was shown to result from the activation of Na+/K+-ATPase via an increase in Na+ influx that is mediated, at least in part, by the stimulation of Na+-dependent amino acid transport. The increased Na+-dependent amino acid uptake by BDNF is followed by an enhancement of overall protein synthesis associated with the differentiation of cortical neurons. Together, these data demonstrate the
Here we evaluated the effects of Tualang honey, a phytoestrogen, and 17 β -estradiol (E2) on the depressive-like behaviour, stress hormones, and BDNF concentration in stressed ovariectomised (OVX) rats. The animals were divided into six groups: (i) nonstressed sham-operated control, (ii) stressed sham-operated control, (iii) nonstressed OVX, (iv) stressed OVX, (v) stressed OVX treated with E2 (20 μ g daily, sc), and (vi) stressed OVX treated with Tualang honey (0.2 g/kg body weight daily, orally). Two months after surgery, the animals were subjected to social instability stress procedure followed by forced swimming test. Struggling time, immobility time, and swimming time were scored. Serum adrenocorticotropic hormone (ACTH) and corticosterone levels, and the BDNF concentration were determined using commercially available ELISA kits. Stressed OVX rats displayed increased depressive-like behaviour with significantly increased serum ACTH and corticosterone levels, while the BDNF concentration ...
Here we evaluated the effects of Tualang honey, a phytoestrogen, and 17 β -estradiol (E2) on the depressive-like behaviour, stress hormones, and BDNF concentration in stressed ovariectomised (OVX) rats. The animals were divided into six groups: (i) nonstressed sham-operated control, (ii) stressed sham-operated control, (iii) nonstressed OVX, (iv) stressed OVX, (v) stressed OVX treated with E2 (20 μ g daily, sc), and (vi) stressed OVX treated with Tualang honey (0.2 g/kg body weight daily, orally). Two months after surgery, the animals were subjected to social instability stress procedure followed by forced swimming test. Struggling time, immobility time, and swimming time were scored. Serum adrenocorticotropic hormone (ACTH) and corticosterone levels, and the BDNF concentration were determined using commercially available ELISA kits. Stressed OVX rats displayed increased depressive-like behaviour with significantly increased serum ACTH and corticosterone levels, while the BDNF concentration ...
We investigated whether δ-opioid receptor (DOR)-induced neuroprotection involves the brain-derived neurotrophic factor (BDNF) pathway. We studied the effect of DOR activation on the expression of BDNF and other proteins in the cortex of C57BL/6 mice exposed to hypoxia (10% of oxygen) for 1-10 days. The results showed that: (1) 1-day hypoxia had no appreciable effect on BDNF expression, while 3- and 10-day hypoxia progressively decreased BDNF expression, resulting in 37.3% reduction (p < 0.05) after 10-day exposure; (2) DOR activation with UFP-512 (1 mg/kg, i.p., daily) partially reversed the hypoxia-induced reduction of BDNF expression in the 3- or 10-day exposed cortex; (3) DOR activation partially reversed the hypoxia-induced reduction in functional TrkB (140-kDa) and attenuated hypoxia-induced increase in truncated TrkB (90-kDa) in the 3- or 10-day hypoxic cortex; and (4) prolonged hypoxia (10 days) significantly increased TNF-α level and decreased CD11b expression in the cortex, which was
Introduction: Alzheimer's disease (AD) is a progressive neurodegenerative disease of the central nervous system. Neuronal injury and oxidative stress in AD increases the level of inflammatory cytokines. Curcumin has antioxidant and neuroprotective properties. The aim of this study was to determine the effect of curcumin on hippocampal levels of brain-derived neurotrophic ...
Could an alternative version of your brain-derived neurotropic factor be an excuse for your failed road test?. According to research published in the Journal, Cerebral Cortex, by Stephanie McHughen et.al., a key SNP in BDNF (valine 66 mutated to methionine) impacts learning and memory functions, cognitive tools which happen to be crucial for operating an automobile.. During one of the described experiments, subjects were seated at a computer, with attached steering wheel as they had to keep the virtual car on a black line in the center of the screen. Subjects got to learn the driving circuit by following the car on 15, 60 second trials. While both groups of subjects (those who had the "normal" valine allele, and those with the val66met SNP) started at similar levels of ability, and showed short term learning. During the trials however, val66met subjects showed less learning, and made more mistakes while learning. By day 5 of training, those with the val66met allele showed less ability to retain ...
Neurotrophic factors have an established developmental role in regulating the survival and specification of sensory neurons. However, these factors continue to exert an important influence on sensory neurons throughout the postnatal period and into adult life. In adulthood, approximately one-half of nociceptors are dependent on nerve growth factor (NGF) for trophic support, whereas the other half are sensitive to glial cell line-derived neurotrophic factor (GDNF). It is now known that many chronic pain states are maintained by widespread changes in the anatomy, neurochemistry, and function of the sensory nervous system both at the level of the primary sensory neuron and the dorsal horn of the spinal cord. Trophic factors appear to orchestrate many of these dynamic changes. This review highlights some of the key roles played by these molecules and in particular the role of NGF in the peripheral sensitization of nociceptors and brain-derived neurotrophic factor (BDNF) as a central pain modulator.
Jusen Tsuru,1 Yoshihiro Tanaka,1 Yoshinobu Ishitobi,1 Yoshihiro Maruyama,1 Ayako Inoue,1 Aimi Kawano,1 Rie Ikeda,1 Tomoko Ando,1 Harumi Oshita,2 Saeko Aizawa,1 Koji Masuda,1 Haruka Higuma,1 Masayuki Kanehisa,1 Taiga Ninomiya,1 Jotaro Akiyoshi1 1Department of Neuropsychiatry, 2Department of Applied Linguistics, Faculty of Medicine, Oita University, Oita, Japan Background: Decreased expression of brain-derived neurotrophic factor (BDNF) is implicated in enhanced stress responses. The BDNF Val66Met polymorphism is associated with psychological changes; for example, carriers of the Met allele exhibit increased harm avoidance as well as a higher prevalence of depression and anxiety disorder.Methods: To analyze the effects of BDNF Val66Met on stress responses, we tested 226 university students (88 women and 138 men) using a social stress procedure (Trier Social Stress Test [TSST]) and an electrical stimulation stress test. Stress indices were derived from repeated measurements of salivary &alpha;
TY - JOUR. T1 - Calcitonin gene-related peptide enhances release of native brain-derived neurotrophic factor from trigeminal ganglion neurons. AU - Buldyrev, Ilya. AU - Tanner, Nathan M.. AU - Hsieh, Hui Ya. AU - Dodd, Emily G.. AU - Nguyen, Loi T.. AU - Balkowiec, Agnieszka. PY - 2006/12/1. Y1 - 2006/12/1. N2 - Activity-dependent plasticity in nociceptive pathways has been implicated in pathomechanisms of chronic pain syndromes. Calcitonin gene-related peptide (CGRP), which is expressed by trigeminal nociceptors, has recently been identified as a key player in the mechanism of migraine headaches. Here we show that CGRP is coexpressed with brain-derived neurotrophic factor (BDNF) in a large subset of adult rat trigeminal ganglion neurons in vivo. Using ELISA in situ, we show that CGRP (1-1000 nm) potently enhances BDNF release from cultured trigeminal neurons. The effect of CGRP is dose-dependent and abolished by pretreatment with CGRP receptor antagonist, CGRP(8-37). Intriguingly, CGRP-mediated ...
Background Human milk contains a wide variety of nutrients that contribute to the fulfillment of its functions, which include the regulation of newborn development. However, few studies have investigated the concentrations of S100B protein, brain-derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF) in human milk. The associations of the concentrations of S100B protein, BDNF, and GDNF with maternal factors are not well explored. Methodology/Principal Findings To investigate the concentrations of S100B protein, BDNF, and GDNF in human milk and characterize the maternal factors associated with their levels in human milk, human milk samples were collected at days 3, 10, 30, and 90 after parturition. Levels of S100B protein, BDNF, and GDNF, and their mRNAs in the samples were detected. Then, these concentrations were compared with lactation and other maternal factors. S100B protein levels in human milk samples collected at 3, 10, 30, and 90 d after parturition were
article{8bf0b2a2-668e-47c2-96c7-c99a9822e436, abstract = {,p,The neurotrophic effects of the BB isoform of platelet-derived growth factor (PDGF) on rat and human fetal mesencephalic dopaminergic neurons have been characterized in vitro. A dose-response analysis demonstrated maximal responses at 30 ng/ml of PDGF-BB. This concentration resulted in a marked increase in the survival and neurite outgrowth from rat and human tyrosine hydroxylase-(TH) positive, presumed dopaminergic neurons after 7 days in vitro. The effects of PDGF-BB on survival of TH-positive neurons were comparable to those of brain-derived neurotrophic factor (BDNF), whereas neurite outgrowth was more pronounced after addition of BDNF. The combination of BDNF and PDGF-BB yielded no additive effects. Double immunohistochemical staining of rat cultures demonstrated PDGF beta-receptors on about 90% of the TH-positive neurons. PDGF-BB treatment of rat mesencephalic cultures induced an upregulation of c-fos and TH mRNA with maximal ...
TY - JOUR. T1 - Administration of a tropomyosin receptor kinase inhibitor attenuates sarcoma-induced nerve sprouting, neuroma formation and bone cancer pain. AU - Ghilardi, Joseph R.. AU - Freeman, Katie T.. AU - Jimenez-Andrade, Juan M.. AU - Mantyh, William G.. AU - Bloom, Aaron P.. AU - Kuskowski, Michael A.. AU - Mantyh, Patrick W. PY - 2010/12/7. Y1 - 2010/12/7. N2 - Pain often accompanies cancer and most current therapies for treating cancer pain have significant unwanted side effects. Targeting nerve growth factor (NGF) or its cognate receptor tropomyosin receptor kinase A (TrkA) has become an attractive target for attenuating chronic pain. In the present report, we use a mouse model of bone cancer pain and examine whether oral administration of a selective small molecule Trk inhibitor (ARRY-470, which blocks TrkA, TrkB and TrkC kinase activity at low nm concentrations) has a significant effect on cancer-induced pain behaviors, tumor-induced remodeling of sensory nerve fibers, tumor ...
It has been shown that the noradrenergic (NE) locus coeruleus (LC)-hippocampal pathway plays an important role in learning and memory processing, and that the development of this transmitter pathway is influenced by neurotrophic factors. Although some of these factors have been discovered, the regulatory mechanisms for this developmental event have not been fully elucidated. Glial cell line-derived neurotrophic factor (GDNF) is a potent neurotrophic factor influencing LC-NE neurons. We have utilized a GDNF knockout animal model to explore its function on the LC-NE transmitter system during development, particularly with respect to target innervation. By transplanting various combinations of brainstem (including LC) and hippocampal tissues from wildtype or GDNF knockout fetuses into the brains of adult wildtype mice, we demonstrate that normal postnatal development of brainstem LC-NE neurons is disrupted as a result of the GDNF null mutation. Tyrosine hydroxylase immunohistochemistry revealed ...
Disclosed are novel proteins, referred to as truncated glial cell line-derived neurotrophic factor (truncated GDNF) proteins, that promote dopamine uptake by dopaminergic cells and promote the survival of nerve cells. Also disclosed are processes for obtaining the truncated GDNF proteins by recombinant genetic engineering techniques.
For years, researchers seeking new therapies for traumatic brain injury have been tantalized by the results of animal experiments with stem cells. In numerous studies, stem cell implantation has substantially improved brain function in experimental animals with brain trauma. But just how these improvements occur has remained a mystery.. Now, an important part of this puzzle has been pieced together by researchers at the University of Texas Medical Branch at Galveston. In experiments with both laboratory rats and an apparatus that enabled them to simulate the impact of trauma on human neurons, they identified key molecular mechanisms by which implanted ...
Purpose: : To report the first case of a neurotrophic keratopathy associated with a trigeminal trophic syndrome. Methods: : A retrospective case study. Results: : A seven- year-old girl presented with a two-week history of redness and decreased vision in her left eye. Her prior medical history was significant for resection of posterior fossa ganglioglioma. On examination she was found to have a large epithelial defect in the left cornea. Her corneal sensation was decreased in the left eye due to CN V deficit related to the brain tumor resection. She was diagnosed with a neurotrophic keratopathy and treated with frequent lubrication and patching. The neurotrophic keratopathy improved gradually with treatment. Two months later, she developed non-healing deep ulcerations on the left side of her nose, and on the eyelid near the left medial canthus. The cultures of the lesions were negative. Due to progressive nature of the facial lesions and tissue destruction, she was referred to dermatology, and ...

Effect of treatment on serum brain-derived neurotrophic factor levels in depressed patients | SpringerLinkEffect of treatment on serum brain-derived neurotrophic factor levels in depressed patients | SpringerLink

Researchers have reported that serum brain-derived neurotrophic factor (sBDNF) of drug-free depressed patients are lower than ... Radka SF, Holst PA, Fritsche M, Atlar CA (1996) Presence of brain-derived neurotrophic factor in brain and human and rat but ... Pan W, Banks WA, Fasold MB, Bluth J, Kastin AJ (1998) Transport of brain-derived neurotrophic factor across the blood-brain ... Karege F, Schwald M, Cisse M (2002b) Postnatal developmental profile of brain-derived neurotrophic factor in rat brain and ...
more infohttps://link.springer.com/article/10.1007%2Fs00406-005-0578-6

S100B Protein, Brain-Derived Neurotrophic Factor, and Glial Cell Line-Derived Neurotrophic Factor in Human MilkS100B Protein, Brain-Derived Neurotrophic Factor, and Glial Cell Line-Derived Neurotrophic Factor in Human Milk

... brain-derived neurotrophic factor (BDNF), and glial cell line-derived neurotrophic factor (GDNF) in human milk. The ... Then, these concentrations were compared with lactation and other maternal factors. S100B protein levels in human milk samples ... and GDNF in human milk and characterize the maternal factors associated with their levels in human milk, human milk samples ... associations of the concentrations of S100B protein, BDNF, and GDNF with maternal factors are not well explored. Methodology/ ...
more infohttp://journals.plos.org/plosone/article?id=10.1371/journal.pone.0021663

HSP105 prevents depression-like behavior by increasing hippocampal brain-derived neurotrophic factor levels in mice | Science...HSP105 prevents depression-like behavior by increasing hippocampal brain-derived neurotrophic factor levels in mice | Science...

HSP105 prevents depression-like behavior by increasing hippocampal brain-derived neurotrophic factor levels in mice ... HSP105 prevents depression-like behavior by increasing hippocampal brain-derived neurotrophic factor levels in mice ... HSP105 prevents depression-like behavior by increasing hippocampal brain-derived neurotrophic factor levels in mice ... HSP105 prevents depression-like behavior by increasing hippocampal brain-derived neurotrophic factor levels in mice ...
more infohttps://advances.sciencemag.org/content/3/5/e1603014/tab-figures-data

Patent US7390781 - Methods of using truncated glial cell line-derived neurotrophic factor - Google PatentsPatent US7390781 - Methods of using truncated glial cell line-derived neurotrophic factor - Google Patents

... referred to as truncated glial cell line-derived neurotrophic factor (truncated GDNF) proteins, that promote dopamine uptake by ... neurotrophic factors such as brain derived neurotrophic factor, neurotrophin-3, neurotrophin-4/5, neurotrophin-6, insulin-like ... referred to herein as glial cell line-derived neurotrophic factors (also referred to as glial derived neurotrophic factor or ... Brain derived neurotrophic factor. WO1991010425A1. Jan 8, 1991. Jul 25, 1991. Brown University Research Foundation. Cell ...
more infohttp://www.google.com/patents/US7390781?dq=6,125,447

Serum brain-derived neurotrophic factor and peripheral indicators of the serotonin system in underweight and weight-recovered...Serum brain-derived neurotrophic factor and peripheral indicators of the serotonin system in underweight and weight-recovered...

Serum brain-derived neurotrophic factor and peripheral indicators of the serotonin system in underweight and weight-recovered ... Serum brain-derived neurotrophic factor and peripheral indicators of the serotonin system in underweight and weight-recovered ... Background: Brain-derived neurotrophic factor (BDNF) mutant mice show hyperphagia and hyperleptinemia. Animal and cell-culture ...
more infohttp://jpn.ca/vol34-issue4/34-4-323/

Brain-derived neurotrophic factor - WikipediaBrain-derived neurotrophic factor - Wikipedia

BDNF, brain-derived neurotrophic factor, ANON2, BULN2, Brain-derived neurotrophic factor, brain derived neurotrophic factor. ... Brain-derived neurotrophic factor, also known as BDNF, is a protein[5] that, in humans, is encoded by the BDNF gene.[6][7] BDNF ... "Brain-derived neurotrophic factor". Growth Factors. 22 (3): 123-31. doi:10.1080/08977190410001723308. PMC 2504526. PMID ... brain-derived neurotrophic factor receptor signaling pathway. • negative regulation of neuron apoptotic process. • synapse ...
more infohttps://en.wikipedia.org/wiki/Brain_derived_neurotrophic_factor

Brain-derived neurotrophic factor - WikipediaBrain-derived neurotrophic factor - Wikipedia

"Brain-derived neurotrophic factor". Growth Factors. 22 (3): 123-31. doi:10.1080/08977190410001723308. PMC 2504526 . PMID ... also known as chemo brain) and fatigue. Epigenetics of depression § Brain-derived neurotrophic factor Epigenetics of ... Brain-derived neurotrophic factor, also known as BDNF, is a protein that, in humans, is encoded by the BDNF gene. BDNF is a ... Wu K, Len GW, McAuliffe G, Ma C, Tai JP, Xu F, Black IB (November 2004). "Brain-derived neurotrophic factor acutely enhances ...
more infohttps://en.wikipedia.org/wiki/Brain-derived_neurotrophic_factor

Mus musculus brain-derived neurotrophic factor precursor transcript va - Nucleotide - NCBIMus musculus brain-derived neurotrophic factor precursor transcript va - Nucleotide - NCBI

Mus musculus brain-derived neurotrophic factor precursor transcript variant IIA ... Mus musculus brain-derived neurotrophic ... Mus musculus brain-derived neurotrophic factor precursor transcript variant IIA (Bdnf) mRNA, complete cds, alternatively ... The protein encoded by this gene is a member of the nerve growth factor family. It is involved in the growth, differentiation ... Delta-secretase-cleaved Tau antagonizes TrkB neurotrophic signalings, mediating Alzheimers disease pathologies. [Proc Natl ...
more infohttps://www.ncbi.nlm.nih.gov/nuccore/EF125670.1

Brain-derived neurotrophic factor and cocaine addiction.  - PubMed - NCBIBrain-derived neurotrophic factor and cocaine addiction. - PubMed - NCBI

Brain Res. 2010 Feb 16;1314:183-93. doi: 10.1016/j.brainres.2009.08.078. Epub 2009 Sep 2. Research Support, N.I.H., Extramural ... The effects of brain-derived neurotrophic factor (BDNF) on cocaine-seeking are brain region-specific. Infusion of BDNF into ... Brain-derived neurotrophic factor and cocaine addiction.. McGinty JF1, Whitfield TW Jr, Berglind WJ. ... Brain Res. 2010 Feb 16;1314:183-93. doi: 10.1016/j.brainres.2009.08.078. Epub 2009 Sep 2. ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/19732758?dopt=Abstract

TrkB-Mediated Neuroprotective and Antihypoxic Properties of Brain-Derived Neurotrophic FactorTrkB-Mediated Neuroprotective and Antihypoxic Properties of Brain-Derived Neurotrophic Factor

"Brain-derived neurotrophic factor messenger RNA is expressed in the septum, hypothalamus and in adrenergic brain stem nuclei of ... "Differential regulation of brain derived neurotrophic factor transcripts by antidepressant treatments in the adult rat brain," ... M. Kairisalo, L. Korhonen, M. Sepp et al., "NF-κB-dependent regulation of brain-derived neurotrophic factor in hippocampal ... T. A. Sakharnova, M. V. Vedunova, and I. V. Mukhina, "Brain-derived neurotrophic factor (BDNF) and its role in the functioning ...
more infohttps://www.hindawi.com/journals/omcl/2015/453901/ref/

What is a Brain-Derived Neurotrophic Factor? (with pictures)What is a Brain-Derived Neurotrophic Factor? (with pictures)

A brain-derived neurotrophic factor is a type of protein that is capable of regulating the development of neurons. In most ... with the assistance of brain-derived neurotrophic factor. Without BDNF, the brain cannot perform a number of important ... Brain-derived neurotrophic factor (BDNF) is a protein capable of regulating the development of neurons. It is found primarily ... Variations in brain-derived neurotrophic factor levels have been linked with neurological diseases, mental illness, and delays ...
more infohttps://www.wisegeek.com/what-is-a-brain-derived-neurotrophic-factor.htm

Brain-derived neurotrophic factor - DrugBankBrain-derived neurotrophic factor - DrugBank

Brain-derived neurotrophic factor. Details. Name. Brain-derived neurotrophic factor. Kind. protein. Organism. Humans. ... Brain-derived neurotrophic factor. P23560. Details. Drug Relations. Drug Relations. DrugBank ID. Name. Drug group. ...
more infohttps://www.drugbank.ca/bio_entities/BE0003394

Brain Derived Neurotrophic Factor ELISA Kits | Biocompare.comBrain Derived Neurotrophic Factor ELISA Kits | Biocompare.com

Compare Brain Derived Neurotrophic Factor ELISA Kits from leading suppliers on Biocompare. View specifications, prices, ... BDNF (Brain Derived Neurotrophic Factor), BioAssay™ ELISA Kit (Human) *Detection Target: BDNF (Brain Derived Neurotrophic ... BDNF (Brain Derived Neurotrophic Factor) BioAssay™ ELISA Kit (Equine) *Detection Target: BDNF (Brain Derived Neurotrophic ... Your search returned 357 Brain Derived Neurotrophic Factor ELISA ELISA Kit across 25 suppliers. ...
more infohttps://www.biocompare.com/pfu/110627/soids/2-341231/Assay_Kit/ELISA_Brain_Derived_Neurotrophic_Factor

Brain-Derived Neurotrophic Factor Regulates Cholesterol Metabolism for Synapse Development | Journal of NeuroscienceBrain-Derived Neurotrophic Factor Regulates Cholesterol Metabolism for Synapse Development | Journal of Neuroscience

Among neurotrophins, brain-derived neurotrophic factor (BDNF) is highly expressed in brain and mediates multiple effects on CNS ... Brain-Derived Neurotrophic Factor Regulates Cholesterol Metabolism for Synapse Development. Shingo Suzuki, Kazuyuki Kiyosue, ... Brain-Derived Neurotrophic Factor Regulates Cholesterol Metabolism for Synapse Development. Shingo Suzuki, Kazuyuki Kiyosue, ... Brain-Derived Neurotrophic Factor Regulates Cholesterol Metabolism for Synapse Development Message Subject (Your Name) has ...
more infohttp://www.jneurosci.org/content/27/24/6417.long

What is the role of brain-derived neurotrophic factor in the pathogenesis of tardive dyskinesia (TD)?What is the role of brain-derived neurotrophic factor in the pathogenesis of tardive dyskinesia (TD)?

Tan et al reported an inverse correlation of plasma levels of brain-derived neurotrophic factor and dyskinetic movements in ... people with schizophrenia who had TD.{ref8} Thus, brain-derived neurotrophic... more ... 8] Thus, brain-derived neurotrophic factor appears to have a protective effect in the nervous system against TD with people ... What is the role of brain-derived neurotrophic factor in the pathogenesis of tardive dyskinesia (TD)?. Updated: Oct 17, 2018 ...
more infohttps://www.medscape.com/answers/1151826-4250/what-is-the-role-of-brain-derived-neurotrophic-factor-in-the-pathogenesis-of-tardive-dyskinesia-td

Brain-Derived Neurotrophic Factor in Obesity and Brain Function - Full Text View - ClinicalTrials.govBrain-Derived Neurotrophic Factor in Obesity and Brain Function - Full Text View - ClinicalTrials.gov

Brain-Derived Neurotrophic Factor in Obesity and Brain Function. This study has been completed. ... These problems may be related to Brain-Derived Neurotrophic Factor (BDNF), a protein that is important for brain development. ... Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also ... Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor. Nat Neurosci. 2003 Jul;6(7): ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01517048?term=overweight+OR+obesity&recr=Open&fund=01&rank=14

Brain-Derived Neurotrophic Factor in Obesity and Brain Function - Full Text View - ClinicalTrials.govBrain-Derived Neurotrophic Factor in Obesity and Brain Function - Full Text View - ClinicalTrials.gov

Brain-Derived Neurotrophic Factor in Obesity and Brain Function. This study has been completed. ... These problems may be related to Brain-Derived Neurotrophic Factor (BDNF), a protein that is important for brain development. ... Brain-derived neurotrophic factor (BDNF) is a protein that is important in nervous system development and function. BDNF also ... Brain-derived neurotrophic factor regulates energy balance downstream of melanocortin-4 receptor. Nat Neurosci. 2003 Jul;6(7): ...
more infohttps://clinicaltrials.gov/ct2/show/NCT01517048?recr=Open&cond=%22Mental+Retardation%22&rank=9

Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor | Journal of NeuroscienceSingle-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor | Journal of Neuroscience

... derived neurotrophic factor-green fluorescent protein suggest an activity-dependent local release of brain-derived neurotrophic ... Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor. Jason P. Magby, Caixia Bi, Zhe-Yu ... Single-Cell Characterization of Retrograde Signaling by Brain-Derived Neurotrophic Factor. Jason P. Magby, Caixia Bi, Zhe-Yu ... Brain-derived neurotrophic factor (BDNF) is a key regulator of hippocampal synaptic plasticity in the developing and adult ...
more infohttp://www.jneurosci.org/content/26/52/13531

brain derived neurotrophic factor Protocols and Video...'brain derived neurotrophic factor' Protocols and Video...

... brain derived neurotrophic factor include Enzyme-linked Receptors, Two-photon Imaging of Microglial Processes Attraction ... Toward ATP or Serotonin in Acute Brain Slices, Presynaptic Dopamine Dynamics in Striatal Brain Slices with Fast-scan Cyclic ... Short-Term Free-Floating Slice Cultures from the Adult Human Brain, Presynapse Formation Assay Using Presynapse Organizer ... Brain-Derived Neurotrophic Factor: A member of the nerve growth factor family of trophic factors. In the brain Bdnf has a ...
more infohttps://www.jove.com/keyword/brain+derived+neurotrophic+factor

Brain-derived neurotrophic factor restores long-term potentiation in polysialic acid-neural cell adhesion molecule-deficient...Brain-derived neurotrophic factor restores long-term potentiation in polysialic acid-neural cell adhesion molecule-deficient...

... and for growth factors (18, 19). Among these, brain-derived neurotrophic factor (BDNF) is certainly one interesting candidate ... brain-derived neurotrophic factor;. PSA,. polysialic acid;. LTP,. long-term potentiation;. TBS,. theta burst stimulation;. EPSP ... can be rescued by brain-derived neurotrophic factor (BDNF). This effect is not reproduced by nerve growth factor, but can be ... Increased Expression of Brain-Derived Neurotrophic Factor Induces Formation of Basal Dendrites and Axonal Branching in Dentate ...
more infohttp://www.pnas.org/content/97/8/4315

An Antioxidant Dietary Supplement Improves Brain-Derived Neurotrophic Factor Levels in Serum of Aged Dogs: Preliminary ResultsAn Antioxidant Dietary Supplement Improves Brain-Derived Neurotrophic Factor Levels in Serum of Aged Dogs: Preliminary Results

"Precursor form of brain-derived neurotrophic factor and mature brain-derived neurotrophic factor are decreased in the pre- ... D. K. Binder and H. E. Scharfman, "Brain-derived neurotrophic factor," Growth Factors, vol. 22, no. 3, pp. 123-131, 2004. View ... "Pro-brain-derived neurotrophic factor is decreased in parietal cortex in Alzheimers disease," Molecular Brain Research, vol. ... refined sugar diet reduces hippocampal brain-derived neurotrophic factor, neuronal plasticity, and learning," Neuroscience, vol ...
more infohttps://www.hindawi.com/journals/jvm/2015/412501/ref/

Reduced serum brain-derived neurotrophic factor in patients with  | NDTReduced serum brain-derived neurotrophic factor in patients with | NDT

... such as brain-derived neurotrophic factor (BDNF), is associated with vitiligo. Patients and methods: This study was conducted ... Reduced serum brain-derived neurotrophic factor in patients with first onset vitiligo M Emin Yanik,1 Gamze Erfan,1 Yakup ... Reduced serum brain-derived neurotrophic factor in patients with first onset vitiligo. ... such as brain-derived neurotrophic factor (BDNF), is associated with vitiligo. Patients and methods: This study was conducted ...
more infohttps://www.dovepress.com/reduced-serum-brain-derived-neurotrophic-factornbspin-patients-with-fi-peer-reviewed-article-NDT

Methamphetamine self-administration attenuates hippocampal serotonergic deficits: role of brain-derived neurotrophic factor. |...Methamphetamine self-administration attenuates hippocampal serotonergic deficits: role of brain-derived neurotrophic factor. |...

Methamphetamine self-administration attenuates hippocampal serotonergic deficits: role of brain-derived neurotrophic factor.. [ ... Previous work also demonstrates that brain-derived neurotrophic factor (BDNF) exposure increases SERT function. The current ...
more infohttps://www.sigmaaldrich.com/catalog/papers/24650575

Possible Role of Brain-Derived Neurotrophic Factor in the Pathogenesis of Coronary Artery Disease | CirculationPossible Role of Brain-Derived Neurotrophic Factor in the Pathogenesis of Coronary Artery Disease | Circulation

Possible Role of Brain-Derived Neurotrophic Factor in the Pathogenesis of Coronary Artery Disease. Junya Ejiri, Nobutaka Inoue ... Possible Role of Brain-Derived Neurotrophic Factor in the Pathogenesis of Coronary Artery Disease ... Possible Role of Brain-Derived Neurotrophic Factor in the Pathogenesis of Coronary Artery Disease ... Possible Role of Brain-Derived Neurotrophic Factor in the Pathogenesis of Coronary Artery Disease ...
more infohttp://circ.ahajournals.org/content/early/2005/09/26/CIRCULATIONAHA.104.476903
  • Dias BG, Banerjee SB, Duman RS, Vaidya VA (2003) Differential regulation of brain derived neurotrophic factor transcripts by antidepressant treatments in the adult rat brain. (springer.com)
  • Dias BG, Banerjee SB, Duman RS, Vaidya VA (2003) Differential regulation of brain derived neurotrophic factor transcripts by antidepressant treatments in the adult rat brain. (springer.com)
  • The rodent retina undergoes considerable postnatal neurogenesis and phenotypic differentiation, and it is likely that diffusible neurotrophic factors contribute to this development and to the subsequent formation of functional retinal circuitry. (uniprot.org)
  • Brain-Derived Neurotrophic Factor in Patients With Age-Related Macular Degeneration and Its Correlation With Retinal Layer Thicknesses. (bioportfolio.com)
  • In spite of our better understanding of several neurobiological alterations in brain structure, physiology and neurochemistry in patients in schizophrenia, there is currently no objective laboratory tool that can be used in the diagnosis, management and prognostication of schizophrenia. (cpn.or.kr)
  • However, individuals without a personal or family history of major depressive disorder tend to not show any mood changes following tryptophan depletion, 8 despite the fact that tryptophan depletion alters the activity of mood-regulating regions of the brain, such as the amygdala, in these individuals as it does in patients with major depressive disorder. (cmaj.ca)
  • Although several genetic variants and vascular risk factors have been linked to mnemonic performance in general and age differences therein, it is unknown whether and how they modify age-related memory declines. (frontiersin.org)
  • Frontotemporal lobar degeneration (FTLD) has a strong genetic background, but genetic risk factors associated with sporadic disease are unknown. (iospress.com)
  • A large number of genetic and environmental factors, most of which remain unknown, likely determine the risk of developing these complex conditions. (nih.gov)
  • Rett syndrome (RTT) is a genetic brain disorder which typically becomes apparent after six months of age in females. (wikipedia.org)
  • Neurological research on humans is hampered by the fact that experimentation on the brain is deemed unethical, forcing researchers to rely on observation and retrospective evaluation to collect data on the role of various compounds in the human brain. (wisegeek.com)
  • One type is primarily trophic and involves long-distance transport of target-derived signals from distal terminals to the nucleus. (jneurosci.org)