A selective and irreversible inhibitor of tryptophan hydroxylase, a rate-limiting enzyme in the biosynthesis of serotonin (5-HYDROXYTRYPTAMINE). Fenclonine acts pharmacologically to deplete endogenous levels of serotonin.
An enzyme that catalyzes the hydroxylation of TRYPTOPHAN to 5-HYDROXYTRYPTOPHAN in the presence of NADPH and molecular oxygen. It is important in the biosynthesis of SEROTONIN.
An enzyme group with broad specificity. The enzymes decarboxylate a range of aromatic amino acids including dihydroxyphenylalanine (DOPA DECARBOXYLASE); TRYPTOPHAN; and HYDROXYTRYPTOPHAN.
A symptom complex associated with CARCINOID TUMOR and characterized by attacks of severe flushing of the skin, diarrheal watery stools, bronchoconstriction, sudden drops in blood pressure, edema, and ascites. The carcinoid tumors are usually located in the gastrointestinal tract and metastasize to the liver. Symptoms are caused by tumor secretion of serotonin, prostaglandins, and other biologically active substances. Cardiac manifestations constitute CARCINOID HEART DISEASE. (Dorland, 27th ed; Stedman, 25th ed)
Works containing information articles on subjects in every field of knowledge, usually arranged in alphabetical order, or a similar work limited to a special field or subject. (From The ALA Glossary of Library and Information Science, 1983)
A biochemical messenger and regulator, synthesized from the essential amino acid L-TRYPTOPHAN. In humans it is found primarily in the central nervous system, gastrointestinal tract, and blood platelets. Serotonin mediates several important physiological functions including neurotransmission, gastrointestinal motility, hemostasis, and cardiovascular integrity. Multiple receptor families (RECEPTORS, SEROTONIN) explain the broad physiological actions and distribution of this biochemical mediator.
An inhibitor of DOPA DECARBOXYLASE that does not enter the central nervous system. It is often given with LEVODOPA in the treatment of parkinsonism to prevent the conversion of levodopa to dopamine in the periphery, thereby increasing the amount that reaches the central nervous system and reducing the required dose. It has no antiparkinson actions when given alone.
A centrally active drug that apparently both blocks serotonin uptake and provokes transport-mediated serotonin release.
A neuronal and epithelial type glutamate plasma membrane transporter protein.
A family of plasma membrane neurotransmitter transporter proteins that couple the uptake of GLUTAMATE with the import of SODIUM ions and PROTONS and the export of POTASSIUM ions. In the CENTRAL NERVOUS SYSTEM they regulate neurotransmission through synaptic reuptake of the excitatory neurotransmitter glutamate. Outside the central nervous system they function as signal mediators and regulators of glutamate metabolism.
Stable cobalt atoms that have the same atomic number as the element cobalt, but differ in atomic weight. Co-59 is a stable cobalt isotope.
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.
Bluish-colored region in the superior angle of the FOURTH VENTRICLE floor, corresponding to melanin-like pigmented nerve cells which lie lateral to the PERIAQUEDUCTAL GRAY.

Behavioral and neurochemical alterations evoked by p-Chlorophenylalanine application in rats examined in the light-dark crossing test. (1/208)

The aim of the present study is to examine the effects of serotonin synthesis inhibition with p-Chlorophenylalanine (p-CPA) in rats on (1) anxiety behavior examined in the light-dark crossing test and, (2) regional brain concentration of monoamines (NA, DA and 5-HT) and their metabolites (MHPG, DOPAC, HVA and 5-HIAA) as well as GABA in the hypothalamus, amygdala, hippocampus, midbrain central gray matter and the frontal cortex. Treatment of animals with p-CPA produced a significant increase in time out from the illuminated part of the chamber and in time of locomotor activity in the illuminated part of the chamber. HPLC analysis showed a significant reduction of 5-HT and 5-HIAA concentration in all examined brain regions with the exception of the frontal cortex. Additionally, a significant decrease in DA and its metabolites, DOPAC and HVA occurred in the hypothalamus and amygdala. Moreover, we observed a significant decrease in frontal cortex NA concentration after p-CPA administration. The results of our study suggest that administration of p-CPA is effective in reduction of anxiety through depletion of 5-HT accompanied by diminution of catecholamines, especially DA and its metabolites in the main emotional brain regions.  (+info)

Sleep and serotonin: an unfinished story. (2/208)

Serotonin (5-HT) was first believed to be a true neuromodulator of sleep because the destruction of 5-HT neurons of the raphe system or the inhibition of 5-HT synthesis with p-chlorophenylalanine induced a severe insomnia which could be reversed by restoring 5-HT synthesis. However the demonstration that the electrical activity of 5-HT perikarya and the release of 5-HT are increased during waking and decreased during sleep was in direct contradiction to this hypothesis. More recent experiments suggest that the release of 5-HT during waking may initiate a cascade of genomic events in some hypnogenic neurons located in the preoptic area. Thus, when 5-HT is released during waking, it leads to an homeostatic regulation of slow-wave sleep.  (+info)

Receptors and neurotransmitters involved in the dual modulation of prolactin release by the serotoninergic system in pregnant and lactating rats. (3/208)

The receptors and neurotransmitter pathways that may participate in the inhibitory action of 5-hydroxytryptamine (5HT) on prolactin release during late pregnancy and lactation in rats were studied. Administration of the 5HT synthesis inhibitor, p-chlorophenylalanine, to late pregnant rats induced a significant increase in serum prolactin concentrations at 17:00 h on day 19 of pregnancy that was partially blocked by injections of the 5HT precursor, 5-hydroxytryptophan, or the 5HT agonists, 8-hydroxy-2-(di-n-propylamino)-tetralin hydrobromide (S1a), 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane (S2) and N-(3-chlorophenyl)imidodicarbonimide diamide HCl (S3), but not by RU 24969 (S1b) or 1-meta-(chlorophenyl)-piperazine-2-HCl (S1a-2c). The 5HT neurotoxins, fenfluramine and p-chloroamphetamine, which selectively destroy fine axon serotoninergic fibres but not coarse ones, prevented the increase in circulating prolactin observed at 18:00 h on pro-oestrus and on day 21 of pregnancy, but did not modify serum prolactin concentrations at 17:00 h on day 19 of pregnancy. Administration of the adrenergic antagonists, metoprolol or prazosin, also prevented the stimulatory effects of p-chlorophenylalanine or ketanserin in pregnant rats on day 19 (17:00 h) or on days 10-12 (16:30 h) in lactating rats separated from their litters. Administration of p-chlorophenylalanine to pregnant rats on day 19 reduced dopamine concentrations in the arcuate nucleus and in the anterior hypothalamus and noradrenaline concentrations in the anterior hypothalamus and the suprachiasmatic nucleus. These results indicate that the inhibitory actions of 5HT on prolactin release in pregnant and lactating rats are mediated by S1a, S2a and S3 receptors and by the coarse axon serotoninergic fibres. In addition, the inhibitory actions of 5HT may modulate the action of a stimulatory adrenergic pathway, as well as the concentrations of noradrenaline and dopamine in different hypothalamic areas, which, in turn, particularly arcuate nucleus dopamine, regulate prolactin release.  (+info)

Serotonin depletion and barrel cortex development: impact of growth impairment vs. serotonin effects on thalamocortical endings. (4/208)

Converging evidence supports a role of serotonin (5-hydroxytryptamine; 5-HT) in barrel cortex development. Systemic administration of 5-HT-depleting drugs reduces cross-sectional whisker barrel areas in the somatosensory cortex (SSC) of neonatal rats. Here we assess the relative impact on barrel pattern formation of (i) 5-HT depletion and (ii) decreased brain growth, which is often associated with pharmacological 5-HT depletion, by comparing the effects of 5-HT-depleting drugs with those of reduced protein intake. Left hemisphere 5-HT levels in the SSC and right hemisphere whisker barrel areas were assessed at postnatal day 6 (P6) in the same animal following injection of p-chloroamphetamine (PCA) or p-chlorophenylalanine (PCPA) at P0. Both drugs significantly reduced cortical 5-HT content and mean barrel areas at P6, but also body and brain growth. Differences in brain weight accounted for 84.4% of the variance in barrel size, with negligible contributions by cortical 5-HT content. PCPA-treated animals sacrificed at P14 yielded similar trends, albeit less pronounced. Finally, reduced protein intake resulted in lower body weight and cortical 5-HT levels at P6, but yielded no change in brain weight or mean barrel area. Barrel formation therefore appears markedly less sensitive to 5-HT depletion per se than to drug-induced growth impairment.  (+info)

Cisplatin-induced early and delayed emesis in the pigeon. (5/208)

1. Intravenously injected cisplatin at a dose of 4 mg kg(-1) induced early and delayed emesis in all pigeons without occurrence of lethality during a 72 h observation period. The early emetic response occurred with a latency of 81.3+/-8.0 min (n=15) and reached a peak at 2 - 3 h, and decreased gradually within 8 h after injection. Then the delayed emetic response, whose peak was found between 10 to 23 h, lasted up to 48 h. The emetic response markedly declined after 48 h. 2. Reserpine markedly reduced monoamine levels in both brain and intestine and completely abolished the early and delayed emesis. Dexamethasone markedly reduced not only the early but also the delayed emetic responses. p-Chlorophenylalanine decreased the level of serotonin in brain and intestine without affecting noradrenaline and dopamine and partly reduced the early emetic response, but did not affect delayed emesis. 3. Bilateral vagotomy prolonged the latency time to the onset of early emesis, and reduced the emetic responses in both the early and delayed phases. 4. The above results suggest that the cisplatin-induced early emesis in the pigeon is partially mediated via the vagal nerve and reserpine-sensitive monoaminergic systems including the serotonergic system; the delayed emesis is associated with monoaminergic but not the serotonergic systems.  (+info)

Endogenous 5-HT tonically inhibits spontaneous firing activity of dorsal hippocampus CA1 pyramidal neurons through stimulation of 5-HT(1A) receptors in quiet awake rats: in vivo electrophysiological evidence. (6/208)

The present study was performed to examine an overall effect of endogenous serotonin (5-HT) on the spontaneous firing activity of the dorsal hippocampus CA1 pyramidal neurons in quiet awake rats. A selective 5-HT(1A) antagonist N-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-N-(2-pyridinyl)cyclohe xanecarboxamide (WAY-100635: 0.03-0.2 mg/kg, s.c.) significantly increased the firing activity. A depletion of 5-HT with parachlorophenylalanine (PCPA: 500 mg/kg/day x 3 days) completely abolished this increasing effect of WAY-100635. The baseline spike frequency of the PCPA-treated rats (3.90 +/- 0.39 Hz) was significantly higher than that of the vehicle-treated rats (2.09 +/- 0.19 Hz). A 5-HT(2A) antagonist ritanserin (1 mg/kg, i.p.) and a 5-HT(3/4) antagonist 2-methoxy-4-amino-5-chloro benzoic acid 2-(diethylamino) ethyl ester (SDZ-205557: 3 mg/kg, s.c.) did not modify the firing activity and the increasing effect of WAY-100635. These results suggest that, in quiet awake rats, endogenous 5-HT would tonically inhibit the spontaneous firing activity of the CA1 pyramidal neurons mainly through stimulating 5-HT(1A) receptors.  (+info)

Brain serotonin dysfunction accounts for aggression in male mice lacking neuronal nitric oxide synthase. (7/208)

Genetically engineered mice with targeted disruption of the neuronal nitric oxide synthase (nNOS) gene established the inhibitory role of nitric oxide (NO) in male impulsive aggressive behavior. This was later confirmed by using selective nNOS inhibitors in male wild-type mice. The molecular mechanisms accounting for the aggressive behavior caused by the lack of neuronally derived NO is not known. Recent studies suggest that central serotonergic neuronal circuits and particularly 5-HT(1A) and 5-HT(1B) receptors play a prominent role in the regulation of aggression. Accordingly, we investigated whether the aggressiveness caused by the lack of nNOS might be because of alterations in serotonergic function. We now demonstrate that the excessive aggressiveness and impulsiveness of nNOS knockout mice is caused by selective decrements in serotonin (5-HT) turnover and deficient 5-HT(1A) and 5-HT(1B) receptor function in brain regions regulating emotion. These results indicate an important role for NO in normal brain 5-HT function and may have significant implications for the treatment of psychiatric disorders characterized by aggressiveness and impulsivity.  (+info)

Reduced brain serotonin activity disrupts prepulse inhibition of the acoustic startle reflex. Effects of 5,7-dihydroxytryptamine and p-chlorophenylalanine. (8/208)

These experiments examined the impact of extensive depletions of forebrain 5-hydroxytryptamine (5-HT; serotonin) levels on prepulse inhibition (PPI) of the acoustic startle reflex in rats. In Experiment 1, injection of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) into the dorsal and median raphe nuclei disrupted PPI. This deficit was observed beginning 2 days after lesioning and was still apparent 8 weeks later. Basal startle reactivity was not altered. The 5-HT(1A) receptor agonist 8-OH-DPAT (0.1 mg/kg) and the dopamine receptor agonist apomorphine (1mg/kg) also disrupted PPI; the effect of 8-OH-DPAT, but not apomorphine, was potentiated in 5-HT-depleted rats. Basal startle reactivity was enhanced by 8-OH-DPAT in sham-lesioned rats but not in 5,7-DHT-lesioned rats. In Experiment 2, a second method for depleting 5-HT was used. The tryptophan hydroxylase inhibitor p-chlorophenylalanine (PCPA) also disrupted PPI without altering basal startle reactivity. Again, 8-OH-DPAT disrupted PPI in control animals; this effect was not altered in PCPA-treated rats but the increase in basal startle reactivity induced by 8-OH-DPAT was not observed in PCPA-treated rats. Taken together with the results of previous experiments involving drugs that enhance 5-HT neurotransmission it appears that both increases and decreases in 5-HT activity disrupt PPI.  (+info)

Fenclonine is not a commonly used medical term or a medication in clinical practice. It's possible that you may have encountered this term in the context of research or scientific studies. Fenclonine is an experimental drug that has been investigated for its potential role as an inhibitor of bacterial enzymes, specifically the D-alanine:D-alanine ligase (DD-transpeptidase) involved in bacterial cell wall biosynthesis.

Inhibiting this enzyme can disrupt the integrity and growth of bacteria, making fenclonine a potential antibiotic agent. However, further research is required to establish its safety, efficacy, and therapeutic applications. As such, it's not currently used as a standard treatment option in human medicine.

For accurate information regarding medical definitions or treatments, consult with healthcare professionals or refer to reputable medical resources.

Tryptophan hydroxylase is an enzyme that plays a crucial role in the synthesis of neurotransmitters and hormones, including serotonin and melatonin. It catalyzes the conversion of the essential amino acid tryptophan to 5-hydroxytryptophan (5-HTP), which is then further converted to serotonin. This enzyme exists in two isoforms, TPH1 and TPH2, with TPH1 primarily located in peripheral tissues and TPH2 mainly found in the brain. The regulation of tryptophan hydroxylase activity has significant implications for mood, appetite, sleep, and pain perception.

Aromatic-L-amino-acid decarboxylases (ALADs) are a group of enzymes that play a crucial role in the synthesis of neurotransmitters and biogenic amines in the body. These enzymes catalyze the decarboxylation of aromatic L-amino acids, such as L-dopa, L-tryptophan, and L-phenylalanine, to produce corresponding neurotransmitters or biogenic amines, including dopamine, serotonin, and histamine, respectively.

There are two main types of ALADs in humans: dopa decarboxylase (DDC) and tryptophan hydroxylase (TPH). DDC is responsible for the conversion of L-dopa to dopamine, which is a crucial neurotransmitter involved in movement regulation. TPH, on the other hand, catalyzes the rate-limiting step in serotonin synthesis by converting L-tryptophan to 5-hydroxytryptophan (5-HTP), which is then converted to serotonin by another enzyme called aromatic amino acid decarboxylase.

Deficiencies or mutations in ALADs can lead to various neurological and psychiatric disorders, such as Parkinson's disease, dopa-responsive dystonia, and depression. Therefore, understanding the function and regulation of ALADs is essential for developing effective therapies for these conditions.

Malignant carcinoid syndrome is a complex of symptoms that occur in some people with malignant tumors (carcinoids) that secrete large amounts of hormone-like substances, particularly serotonin. These symptoms can include flushing of the face and upper body, diarrhea, rapid heartbeat, difficulty breathing, and abdominal pain and distention. In addition, these individuals may have chronic inflammation of the heart valves (endocarditis) leading to heart failure. It is important to note that not all people with carcinoid tumors will develop malignant carcinoid syndrome, but those who do require specific treatment for their symptoms and hormonal imbalances.

An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.

Serotonin, also known as 5-hydroxytryptamine (5-HT), is a monoamine neurotransmitter that is found primarily in the gastrointestinal (GI) tract, blood platelets, and the central nervous system (CNS) of humans and other animals. It is produced by the conversion of the amino acid tryptophan to 5-hydroxytryptophan (5-HTP), and then to serotonin.

In the CNS, serotonin plays a role in regulating mood, appetite, sleep, memory, learning, and behavior, among other functions. It also acts as a vasoconstrictor, helping to regulate blood flow and blood pressure. In the GI tract, it is involved in peristalsis, the contraction and relaxation of muscles that moves food through the digestive system.

Serotonin is synthesized and stored in serotonergic neurons, which are nerve cells that use serotonin as their primary neurotransmitter. These neurons are found throughout the brain and spinal cord, and they communicate with other neurons by releasing serotonin into the synapse, the small gap between two neurons.

Abnormal levels of serotonin have been linked to a variety of disorders, including depression, anxiety, schizophrenia, and migraines. Medications that affect serotonin levels, such as selective serotonin reuptake inhibitors (SSRIs), are commonly used to treat these conditions.

Benserazide is a type of medication called an inhibitor of peripheral aromatic amino acid decarboxylase. It is often used in combination with levodopa to treat Parkinson's disease. Benserazide works by preventing the conversion of levodopa to dopamine outside of the brain, which helps to reduce the side effects of levodopa and increase the amount of dopamine that reaches the brain. This can help to improve the symptoms of Parkinson's disease, such as stiffness, tremors, and difficulty with movement.

Benserazide is available in combination with levodopa under the brand name Madopar. It is taken orally, usually in the form of tablets. The specific dosage of benserazide will depend on the individual's needs and should be determined by a healthcare professional.

It is important to note that benserazide can interact with other medications, so it is important to inform your doctor about all the medications you are taking before starting treatment with benserazide. Additionally, benserazide may cause side effects, such as nausea, dizziness, and dry mouth. If you experience any severe or persistent side effects while taking benserazide, you should contact your healthcare provider.

Fenfluramine is a drug that was previously used for the short-term treatment of obesity. It works by suppressing appetite and increasing the feeling of fullness. Fenfluramine is an amphetamine derivative and stimulates the release of serotonin, a neurotransmitter in the brain that helps regulate mood, appetite, and sleep.

Fenfluramine was commonly prescribed in combination with phentermine, another appetite suppressant, under the brand name Fen-Phen. However, in 1997, the U.S. Food and Drug Administration (FDA) issued a public health warning about the potential risk of serious heart valve damage associated with the use of fenfluramine and withdrew its approval for the drug's use. Since then, fenfluramine has not been approved for medical use in many countries, including the United States.

Excitatory Amino Acid Transporter 3 (EAAT3) is a type of glutamate transporter protein, which is responsible for removing the excitatory neurotransmitter glutamate from the synaptic cleft in the central nervous system. EAAT3 is primarily located on the plasma membrane of neurons and to some extent on astrocytes. It plays a crucial role in maintaining proper glutamate concentration levels in the extracellular space, preventing excitotoxicity and ensuring normal neurotransmission. Mutations in the gene that encodes EAAT3 (SLC1A1) have been associated with neurological disorders such as episodic ataxia, amyotrophic lateral sclerosis, and mood disorders.

Glutamate plasma membrane transport proteins, also known as excitatory amino acid transporters (EAATs), are a type of membrane protein responsible for the uptake of glutamate from the extracellular space into neurons and glial cells in the central nervous system. These transporters play a crucial role in maintaining appropriate levels of glutamate, an important neurotransmitter, in the synaptic cleft to prevent excitotoxicity and ensure normal neurotransmission. There are five subtypes of EAATs (EAAT1-EAAT5) identified in mammals, each with distinct expression patterns and functions.

Cobalt isotopes are variants of the chemical element Cobalt (Co) that have different numbers of neutrons in their atomic nuclei. This results in the different isotopes having slightly different masses and varying levels of stability.

The most naturally occurring stable cobalt isotope is Co-59, which contains 27 neutrons in its nucleus. However, there are also several radioactive isotopes of cobalt, including Co-60, which is a commonly used medical and industrial radioisotope.

Co-60 has 30 neutrons in its nucleus and undergoes beta decay, emitting gamma rays and becoming Nickel-60. It has a half-life of approximately 5.27 years, making it useful for a variety of applications, including cancer treatment, industrial radiography, and sterilization of medical equipment.

Other radioactive isotopes of cobalt include Co-57, which has a half-life of 271.8 days and is used in medical imaging, and Co-56, which has a half-life of just 77.2 seconds and is used in research.

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

The locus coeruleus (LC) is a small nucleus in the brainstem, specifically located in the rostral pons and dorsal to the fourth ventricle. It is the primary site of noradrenaline (norepinephrine) synthesis, storage, and release in the central nervous system. The LC projects its neuronal fibers widely throughout the brain, including the cerebral cortex, thalamus, hippocampus, amygdala, and spinal cord. It plays a crucial role in various physiological functions such as arousal, attention, learning, memory, stress response, and regulation of the sleep-wake cycle. The LC's activity is associated with several neurological and psychiatric conditions, including anxiety disorders, depression, post-traumatic stress disorder (PTSD), and neurodegenerative diseases like Parkinson's and Alzheimer's disease.

... , also known as para-chlorophenylalanine (PCPA), acts as a selective and irreversible inhibitor of tryptophan ... The effects of serotonin depletion from fenclonine are so drastic that serotonin cannot even be detected immunohistochemically ... α-Methyl-para-tyrosine (AMPT, metirosine) para-Chloroamphetamine (PCA) Telotristat ethyl (Xermelo) AGN-2979 "Fenclonine" entry ...
Ketotifen Fenclonine (para-chlorophenylalanine; PCPA) An inhibitor of serotonin synthesis that has been used in the treatment ...
Cremata VY, Koe BK (May 1968). "Clinical and biochemical effects of fenclonine: a serotonin depletor". Diseases of the Nervous ... In a study investigating the effects of Fenclonine on humans, the greatly lowered serotonin levels were associated with " ... especially p-chlorophenylalanine aka PCPA and Fenclonine) has allowed researchers to investigate the effects of very low ...
Administration of fenclonine (para-chlorophenylalanine) is able to bring about a depletion of 5-HT. The mechanism of action for ...
... may refer to: para-Chlorophenylalanine (fenclonine), a synthetic amino acid Premature cleavage and polyadenylation para- ...
... fenclonine MeSH D12.125.072.050.685.450 - p-fluorophenylalanine MeSH D12.125.072.050.685.500 - melphalan MeSH D12.125.072.050. ...
... fenclonine (INN) fenclorac (INN) fenclozic acid (INN) fendiline (INN) fendosal (INN) feneritrol (INN) fenestrel (INN) ...
... para-chloro-phenylalanine or fenclonine (PCPA) pCPP, para-Chlorophenylpiperazine PGP (disambiguation) This disambiguation page ...
Fenclonine, also known as para-chlorophenylalanine (PCPA), acts as a selective and irreversible inhibitor of tryptophan ... The effects of serotonin depletion from fenclonine are so drastic that serotonin cannot even be detected immunohistochemically ... α-Methyl-para-tyrosine (AMPT, metirosine) para-Chloroamphetamine (PCA) Telotristat ethyl (Xermelo) AGN-2979 "Fenclonine" entry ...
TY - JOUR. T1 - Pharmacological modulation of behaviour, serotonin and dopamine levels in daphnia magna exposed to the monoamine oxidase inhibitor deprenyl. AU - Bellot, Marina. AU - Faria, Melissa. AU - Gómez-Canela, Cristian. AU - Raldúa, Demetrio. AU - Barata, Carlos. N1 - Funding Information: Funding: This work was supported by "Agencia Estatal de Investigación" from the Spanish Ministry of Science and Innovation (project PID2020-113371RB-C21), IDAEA-CSIC, Severo Ochoa Centre of Excellence (CEX2018-000794-S), which financed M.F. with Severo Ochoa funds. The work was partially supported by the Catalan Government through the network of recognized research groups (2017 SGR_902). Publisher Copyright: © 2021 by the authors. Licensee MDPI, Basel, Switzerland.. PY - 2021/8. Y1 - 2021/8. N2 - This study assessed the effects of the monoamine oxidase (MAO) inhibitor deprenyl in Daphnia magna locomotor activity. The mechanisms of action of deprenyl were also determined by studying the relationship ...
Fenclonine, Fenfluramine, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Oncogene Proteins v-fos, ...
p-Chlorophenylalanine use Fenclonine P-Component, Serum Amyloid use Serum Amyloid P-Component ...
Fenclonine • Ibopamine • L-DOPA (Levodopa) • L-DOPS (Droxidopa) • L-Phenylalanine • L-Tyrosine • meta-Octopamine • meta- ...
p-Chlorophenylalanine use Fenclonine P-Component, Serum Amyloid use Serum Amyloid P-Component ...
p-Chlorophenylalanine use Fenclonine P-Component, Serum Amyloid use Serum Amyloid P-Component ...
p-Chlorophenylalanine use Fenclonine P-Component, Serum Amyloid use Serum Amyloid P-Component ...
p-Chlorophenylalanine use Fenclonine P-Component, Serum Amyloid use Serum Amyloid P-Component ...
fenclonine (fen′klo-nen). A serotonin inhibitor. Fendt. H., 19th century Austrian dermatologist. See cutaneous pseudolymphoma, ...
Fenclonine / pharmacology* Actions. * Search in PubMed * Search in MeSH * Add to Search ...
... fenclonine and R o-4 -4602 treated animals revealed the ability synthesize 5-hydroxytryptamine (5-HT) and the presence of ...
Fenclonine / pharmacology* Actions. * Search in PubMed * Search in MeSH * Add to Search ...
Fenclonine (L)-Isomer Fenclonine Hydrobromide Fenclonine Hydrochloride Fenclonine, (D)-Isomer p-Chlorophenylalanine para- ... Fenclonine (L)-Isomer Narrower Concept UI. M0329930. Registry Number. 14173-39-8. Terms. Fenclonine (L)-Isomer Preferred Term ... Fenclonine, (D)-Isomer Narrower Concept UI. M0329929. Registry Number. 14091-08-8. Terms. Fenclonine, (D)-Isomer Preferred Term ... Fenclonine Hydrobromide Narrower Concept UI. M0329934. Registry Number. 55327-86-1. Terms. Fenclonine Hydrobromide Preferred ...
Fenclonine (L)-Isomer Fenclonine Hydrobromide Fenclonine Hydrochloride Fenclonine, (D)-Isomer p-Chlorophenylalanine para- ... Fenclonine (L)-Isomer Narrower Concept UI. M0329930. Registry Number. 14173-39-8. Terms. Fenclonine (L)-Isomer Preferred Term ... Fenclonine, (D)-Isomer Narrower Concept UI. M0329929. Registry Number. 14091-08-8. Terms. Fenclonine, (D)-Isomer Preferred Term ... Fenclonine Hydrobromide Narrower Concept UI. M0329934. Registry Number. 55327-86-1. Terms. Fenclonine Hydrobromide Preferred ...
Fenclonine *Para-chlorophenylalanine. *P-chlorophenylalanine. *Dl-3-(4-chlorophenyl)alanine. p-Fluorophenylalanine *P- ...
Fenclonine (L)-Isomer. Fenclonine Hydrobromide. Fenclonine Hydrochloride. Fenclonine, (D)-Isomer. Hydrobromide, Fenclonine. ... Fenclonine - Preferred Concept UI. M0015725. Scope note. A selective and irreversible inhibitor of tryptophan hydroxylase, a ... Fenclonine Entry term(s). DL-3-(4-Chlorophenyl)alanine Fenclonin p-Chlorophenylalanine para Chlorophenylalanine para- ... Hydrochloride, Fenclonine. p-Chlorophenylalanine. para Chlorophenylalanine. para-Chlorophenylalanine. Tree number(s):. D12.125. ...
Molecular brain research, Carrillo A J, Chemical, Depression, Dluzen D E, Dopamine/metabolism, Fenclonine/*pharmacology, Gene ... Fenclonine/*pharmacology, General pharmacology, Inbred Strains, Male, Rats, Schechter M D, Serotonin Antagonists/*pharmacology ...
BV3N6F82WN FENCLEXONIUM C72777 88M0X6627K FENCLEXONIUM METILSULFATE C65642 Y01JW64D01 FENCLOFENAC C65643 R5J7E3L9SP FENCLONINE ...
ENZYME INHIBITORS FENCLONINE ENZYME INHIBITORS FENITROTHION ENZYME INHIBITORS FENOPROFEN ENZYME INHIBITORS FENTHION ENZYME ... SEROTONIN AGENTS FENCLONINE SEROTONIN AGENTS FENFLURAMINE SEROTONIN AGENTS FLUOXETINE SEROTONIN AGENTS FLUVOXAMINE SEROTONIN ... SEROTONIN ANTAGONISTS FENCLONINE SEROTONIN ANTAGONISTS GRANISETRON SEROTONIN ANTAGONISTS KETANSERIN SEROTONIN ANTAGONISTS ... NEUROTRANSMITTER AGENTS FENCLONINE NEUROTRANSMITTER AGENTS FENFLURAMINE NEUROTRANSMITTER AGENTS FENITROTHION NEUROTRANSMITTER ...
  • Fenclonine, also known as para-chlorophenylalanine (PCPA), acts as a selective and irreversible inhibitor of tryptophan hydroxylase, which is a rate-limiting enzyme in the biosynthesis of serotonin. (wikipedia.org)
  • The effects of serotonin depletion from fenclonine are so drastic that serotonin cannot even be detected immunohistochemically within the first day after administration of a control dose. (wikipedia.org)
  • Fenclonine acts pharmacologically to deplete endogenous levels of serotonin. (nih.gov)
  • α-Methyl-para-tyrosine (AMPT, metirosine) para-Chloroamphetamine (PCA) Telotristat ethyl (Xermelo) AGN-2979 "Fenclonine" entry in Martindale - The Complete Drug Reference. (wikipedia.org)