Biogenic amines having only one amine moiety. Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids.
Cell surface proteins that bind biogenic amines with high affinity and regulate intracellular signals which influence the behavior of cells. Biogenic amine is a chemically imprecise term which, by convention, includes the catecholamines epinephrine, norepinephrine, and dopamine, the indoleamine serotonin, the imidazolamine histamine, and compounds closely related to each of these.
A group of naturally occurring amines derived by enzymatic decarboxylation of the natural amino acids. Many have powerful physiological effects (e.g., histamine, serotonin, epinephrine, tyramine). Those derived from aromatic amino acids, and also their synthetic analogs (e.g., amphetamine), are of use in pharmacology.
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 alpha-adrenergic sympathomimetic amine, biosynthesized from tyramine in the CNS and platelets and also in invertebrate nervous systems. It is used to treat hypotension and as a cardiotonic. The natural D(-) form is more potent than the L(+) form in producing cardiovascular adrenergic responses. It is also a neurotransmitter in some invertebrates.
Hydroxyindoleacetic acid (HIAA) is a metabolite of the amino acid tryptophan that is excreted in the urine and can be used as a diagnostic marker for pheochromocytoma, a rare tumor of the adrenal gland.
A family of vesicular amine transporter proteins that catalyze the transport and storage of CATECHOLAMINES and indolamines into SECRETORY VESICLES.
Integral membrane proteins of the LIPID BILAYER of SECRETORY VESICLES that catalyze transport and storage of biogenic amine NEUROTRANSMITTERS such as ACETYLCHOLINE; SEROTONIN; MELATONIN; HISTAMINE; and CATECHOLAMINES. The transporters exchange vesicular protons for cytoplasmic neurotransmitters.
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.
An indirect sympathomimetic. Tyramine does not directly activate adrenergic receptors, but it can serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals. Tyramine may be a neurotransmitter in some invertebrate nervous systems.
An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.
Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic.
A deaminated metabolite of LEVODOPA.
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.
Homovanillic acid (HVA) is a neurotransmitter breakdown product that is measured in the cerebrospinal fluid to help diagnose and monitor conditions such as Parkinson's disease and schizophrenia.
A group of compounds that are methyl derivatives of the amino acid TYROSINE.
An enzyme that catalyzes the oxidative deamination of naturally occurring monoamines. It is a flavin-containing enzyme that is localized in mitochondrial membranes, whether in nerve terminals, the liver, or other organs. Monoamine oxidase is important in regulating the metabolic degradation of catecholamines and serotonin in neural or target tissues. Hepatic monoamine oxidase has a crucial defensive role in inactivating circulating monoamines or those, such as tyramine, that originate in the gut and are absorbed into the portal circulation. (From Goodman and Gilman's, The Pharmacological Basis of Therapeutics, 8th ed, p415) EC 1.4.3.4.
A group of compounds derived from ammonia by substituting organic radicals for the hydrogens. (From Grant & Hackh's Chemical Dictionary, 5th ed)
Biogenic amines having more than one amine group. These are long-chain aliphatic compounds that contain multiple amino and/or imino groups. Because of the linear arrangement of positive charge on these molecules, polyamines bind electrostatically to ribosomes, DNA, and RNA.
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.
A chemically heterogeneous group of drugs that have in common the ability to block oxidative deamination of naturally occurring monoamines. (From Gilman, et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 8th ed, p414)

Ethanol exposure differentially alters central monoamine neurotransmission in alcohol-preferring versus -nonpreferring rats. (1/446)

Individual differences in ethanol preference may be linked to differences in the functional activity of forebrain monoamine systems or their sensitivity to modification by ethanol. To test this hypothesis, basal extracellular concentrations of dopamine (DA) and serotonin (5-HT) in the nucleus accumbens as well as the effects of repeated ethanol pretreatment on the basal release of these transmitters were examined in alcohol-preferring (P), alcohol-nonpreferring (NP), and genetically heterogeneous Wistar rats. All animals received i.p. injections of ethanol (1.0 g/kg) or saline for 5 consecutive days. Fifteen hours after the final pretreatment, basal extracellular concentrations and "in vivo extraction fraction" values for DA and 5-HT were determined by no-net-flux in vivo microdialysis. In ethanol-naive rats, significant line differences were observed with high basal 5-HT release in P rats, low 5-HT release in NP rats, and intermediate 5-HT levels in Wistar rats. No differences among groups were noted in basal DA release. Ethanol pretreatment decreased basal extracellular 5-HT levels in P rats whereas increasing 5-HT efflux was seen in the Wistar and NP lines. In addition, ethanol pretreatment increased extracellular DA concentrations in Wistar and P rats, but not in NP rats. The results confirm a relationship between the functional status of forebrain DA and 5-HT systems and ethanol preference or aversion. Moreover, the data suggest that ethanol exposure can alter basal DA and 5-HT in the nucleus accumbens and that vulnerability to ethanol-induced changes in monoamine neurotransmission may be a factor in genetically determined ethanol preference.  (+info)

Improvement by nefiracetam of beta-amyloid-(1-42)-induced learning and memory impairments in rats. (2/446)

1. We have previously demonstrated that continuous i.c.v. infusion of amyloid beta-peptide (A beta), the major constituent of senile plaques in the brains of patients with Alzheimer's disease, results in learning and memory deficits in rats. 2. In the present study, we investigated the effects of nefiracetam [N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl) acetamide, DM-9384] on A beta-(1-42)-induced learning and memory deficits in rats. 3. In the A beta-(1-42)-infused rats, spontaneous alternation behaviour in a Y-maze task, spatial reference and working memory in a water maze task, and retention of passive avoidance learning were significantly impaired as compared with A beta-(40-1)-infused control rats. 4. Nefiracetam, at a dose range of 1-10 mg kg(-1), improved learning and memory deficits in the A beta-(1-42)-infused rats when it was administered p.o. 1 h before the behavioural tests. 5. Nefiracetam at a dose of 3 mg kg(-1) p.o. increased the activity of choline acetyltransferase in the hippocampus of A beta-(1-42)-infused rats. 6. Nefiracetam increased dopamine turnover in the cerebral cortex and striatum of A beta-(1-42)-infused rats, but failed to affect the noradrenaline, serotonin and 5-hydroxyindoleacetic acid content. 7. These results suggest that nefiracetam may be useful for the treatment of patients with Alzheimer's disease.  (+info)

Dissociable deficits in the decision-making cognition of chronic amphetamine abusers, opiate abusers, patients with focal damage to prefrontal cortex, and tryptophan-depleted normal volunteers: evidence for monoaminergic mechanisms. (3/446)

We used a novel computerized decision-making task to compare the decision-making behavior of chronic amphetamine abusers, chronic opiate abusers, and patients with focal lesions of orbital prefrontal cortex (PFC) or dorsolateral/medial PFC. We also assessed the effects of reducing central 5-hydroxytryptamine (5-HT) activity using a tryptophan-depleting amino acid drink in normal volunteers. Chronic amphetamine abusers showed suboptimal decisions (correlated with years of abuse), and deliberated for significantly longer before making their choices. The opiate abusers exhibited only the second of these behavioral changes. Importantly, both sub-optimal choices and increased deliberation times were evident in the patients with damage to orbitofrontal PFC but not other sectors of PFC. Qualitatively, the performance of the subjects with lowered plasma tryptophan was similar to that associated with amphetamine abuse, consistent with recent reports of depleted 5-HT in the orbital regions of PFC of methamphetamine abusers. Overall, these data suggest that chronic amphetamine abusers show similar decision-making deficits to those seen after focal damage to orbitofrontal PFC. These deficits may reflect altered neuromodulation of the orbitofrontal PFC and interconnected limbic-striatal systems by both the ascending 5-HT and mesocortical dopamine (DA) projections.  (+info)

Differential c-Fos expression in cholinergic, monoaminergic, and GABAergic cell groups of the pontomesencephalic tegmentum after paradoxical sleep deprivation and recovery. (4/446)

Multiple lines of evidence indicate that neurons within the pontomesencephalic tegmentum are critically involved in the generation of paradoxical sleep (PS). From single-unit recording studies, evidence suggests that unidentified but "possibly" cholinergic tegmental neurons discharge at higher rates during PS than during slow wave sleep or even waking and would thus play an active role, whereas "presumed" monoaminergic neurons cease firing during PS and would thus play a permissive role in PS generation. In the present study performed on rats, c-Fos immunostaining was used as a reflection of neuronal activity and combined with immunostaining for choline acetyltransferase (ChAT), serotonin (Ser), tyrosine hydroxylase (TH), or glutamic acid decarboxylase (GAD) for immunohistochemical identification of active neurons during PS recovery ( approximately 28% of recording time) as compared with PS deprivation (0%) and PS control (approximately 15%) conditions. With PS recovery, there was a significant increase in ChAT+/c-Fos+ cells, a significant decrease in Ser+/c-Fos+ and TH+/c-Fos+ cells, and a significant increase in GAD+/c-Fos+ cells. Across conditions, the percent PS was correlated positively with tegmental cholinergic c-Fos+ cells, negatively with raphe serotonergic and locus coeruleus noradrenergic c-Fos+ cells, and positively with codistributed and neighboring GABAergic c-Fos+ cells. These results support the hypothesis that cholinergic neurons are active, whereas monoaminergic neurons are inactive during PS. They moreover indicate that GABAergic neurons are active during PS and could thus be responsible for inhibiting neighboring monoaminergic neurons that may be essential in the generation of PS.  (+info)

Behavioral and neurochemical alterations evoked by p-Chlorophenylalanine application in rats examined in the light-dark crossing test. (5/446)

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)

Cerebrospinal fluid monoaminergic metabolites differ in wild anubis and hybrid (Anubis hamadryas) baboons: possible relationships to life history and behavior. (6/446)

The article reports monoaminergic metabolite [homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HIAA), and 3-methoxy-4-hydroxyphenylglycol (MHPG)], values from the cerebrospinal fluid (CSF) of 27 wild baboons (Papio hamadryas) aged 40 to 140 months. Animals were either anubis, or anubis with hamadryas admixture; males of the latter subspecies generally have a reduced tendency to disperse from their natal groups. Overall, the values and interrelationships among the CSF monoamine metabolites resembled data reported from closely related, captive-housed animals. For example, age was significantly correlated with HVA concentrations (r = -60, p < .05), but not with the other metabolites. Notably, males characterized by hamadryas admixture had significantly higher concentrations of HVA, 5-HIAA, and MHPG (p < .05, respectively), a result possibly driven by differences in serotonergic activity. These data provide initial evidence that variation in central monoaminergic activity, as indicated by CSF monoamine metabolite concentrations, may reflect differences in behavior and life history that have taxonomic and, perhaps, evolutionary significance.  (+info)

Heat shock protein expression protects against cerebral ischemia and monoamine overload in rat heatstroke. (7/446)

This study attempted to ascertain whether the ischemic damage to neurons and monoamine overload in brain that occur during rat heatstroke can be attenuated by heat shock protein (HSP) 72 induction. Effects of heatstroke on mean arterial pressure (MAP), cerebral blood flow (CBF), brain dopamine (DA) and serotonin (5-HT) release, and neural damage score were assayed in rats 0, 16, or 48 h after heat shock (42 degrees C for 15 min) or chemical stress (5 mg/kg sodium arsenite ip). Brain HSP 72 in rats after heat shock or chemical stress was detected by Western blot, and brain monoamine was determined by a microdialysis probe combined with high-performance liquid chromatography. Heatstroke was induced by exposing the animal to a high ambient temperature (43 degrees C); the moment at which MAP and CBF decreased from their peak values was taken as the time of heatstroke onset. Prior heat shock or chemical stress conferred significant protection against heatstroke-induced hyperthermia, arterial hypotension, cerebral ischemia, cerebral DA and 5-HT overload, and neural damage and correlated with expression of HSP 72 in brain at 16 h. However, at 48 h, when HSP 72 expression returned to basal values, the above responses that occurred during the onset of heatstroke were indistinguishable between the two groups (0 h vs. 48 h). These results lead to the hypothesis that the brain can be preconditioned by thermal or chemical injury, that this preconditioning will induce HSP 72, and that HSP 72 induction will correlate quite well with anatomic, histochemical, and hemodynamic protection in rat heatstroke.  (+info)

Sensitization to the effects of tumor necrosis factor-alpha: neuroendocrine, central monoamine, and behavioral variations. (8/446)

Consistent with the proposition that cytokines act as immunotransmitters between the immune system and the brain, systemic administration of the proinflammatory cytokine tumor necrosis factor-alpha (TNF-alpha; 1.0-4.0 microg) induced mild illness in CD-1 mice, increased plasma corticosterone concentrations, and altered central norepinephrine, dopamine, and serotonin turnover. The actions of TNF-alpha were subject to a time-dependent sensitization effect. After reexposure to a subeffective dose of the cytokine (1.0 microgram) 14-28 d after initial treatment, marked illness was evident (reduced consumption of a palatable substance and diminished activity and social exploration), coupled with an elevation of plasma corticosterone levels. In contrast, cytokine reexposure 1-7 d after initial treatment did not elicit illness, and at the 1 d interval the corticosterone response to the cytokine was reduced. The increase of norepinephrine release within the paraventricular nucleus of the hypothalamus, as reflected by elevated accumulation of 3-methoxy-4-hydroxyphenylglycol, was augmented at the longer reexposure intervals. In contrast, within the central amygdala and the prefrontal cortex TNF-alpha reexposure at the 1 d interval was associated with a pronounced sensitization-like effect, which was not apparent at longer intervals. Evidently, systemic TNF-alpha proactively influences the response to subsequent treatment; however, the nature of the effects (i.e., the behavioral, neuroendocrine, and central transmitter alterations) vary over time after initial cytokine treatment. It is suggested that the sensitization may have important repercussions with respect to cognitive effects of TNF-alpha and may also be relevant to analyses of the neuroprotective or neurodestructive actions of cytokines.  (+info)

Biogenic monoamines are a group of neurotransmitters that are synthesized from amino acids in the brain and other tissues. They include dopamine, serotonin, norepinephrine, epinephrine, and histamine. These neurotransmitters play important roles in regulating mood, motivation, attention, and other cognitive and emotional processes. Imbalances in the levels of biogenic monoamines have been implicated in a variety of neurological and psychiatric disorders, including depression, anxiety, and schizophrenia.

Receptors, biogenic amine are proteins found on the surface of cells that bind to biogenic amines, which are neurotransmitters and hormones that are produced in the body. These receptors play a crucial role in regulating various physiological processes, including mood, appetite, and blood pressure. There are several different types of biogenic amine receptors, including dopamine receptors, serotonin receptors, and norepinephrine receptors, each of which has a specific function and can be targeted by drugs to treat various medical conditions.

Biogenic amines are organic compounds that are produced by living organisms, including humans. They are derived from amino acids and are involved in a variety of physiological processes, including neurotransmission, hormone release, and regulation of blood pressure. In the medical field, biogenic amines are often studied in relation to various diseases and disorders. For example, high levels of certain biogenic amines, such as dopamine and norepinephrine, have been linked to conditions such as Parkinson's disease and hypertension. On the other hand, low levels of certain biogenic amines, such as serotonin, have been associated with depression and anxiety disorders. In addition, biogenic amines are also used as diagnostic tools in medical testing. For example, the measurement of levels of certain biogenic amines in the blood or urine can be used to help diagnose and monitor certain diseases, such as pheochromocytoma (a tumor of the adrenal gland) or carcinoid syndrome (a condition caused by the overproduction of certain hormones). Overall, biogenic amines play important roles in many physiological processes and are the subject of ongoing research in the medical field.

Serotonin is a neurotransmitter, a chemical messenger that transmits signals between nerve cells in the brain and throughout the body. It plays a crucial role in regulating mood, appetite, sleep, and other bodily functions. In the medical field, serotonin is often studied in relation to mental health conditions such as depression, anxiety, and obsessive-compulsive disorder (OCD). Low levels of serotonin have been linked to these conditions, and medications such as selective serotonin reuptake inhibitors (SSRIs) are often prescribed to increase serotonin levels in the brain and improve symptoms. Serotonin is also involved in the regulation of pain perception, blood pressure, and other bodily functions. Imbalances in serotonin levels have been implicated in a variety of medical conditions, including migraines, fibromyalgia, and irritable bowel syndrome (IBS).

Octopamine is a biogenic amine that is found in a variety of organisms, including insects, crustaceans, and cephalopods. In the medical field, octopamine is primarily studied for its role in the regulation of various physiological processes, including metabolism, heart rate, and muscle contraction. In insects, octopamine is involved in the control of flight and other behaviors, and it has been shown to play a role in the regulation of feeding and digestion. In crustaceans, octopamine is involved in the control of movement and has been shown to play a role in the regulation of heart rate and blood pressure. In cephalopods, octopamine is involved in the control of muscle contraction and has been shown to play a role in the regulation of feeding and digestion. It is also thought to play a role in the control of behavior and may be involved in the regulation of mood and anxiety. Overall, octopamine is a complex molecule that has a wide range of effects on various physiological processes in different organisms. Further research is needed to fully understand its role in the body and to develop potential therapeutic applications.

Hydroxyindoleacetic acid (HIAA) is a metabolite of the amino acid tryptophan. It is produced in the body by the enzyme indoleamine 2,3-dioxygenase (IDO), which is primarily found in immune cells and the liver. HIAA is excreted in the urine and can be measured in laboratory tests. In the medical field, HIAA is often used as a diagnostic marker for pheochromocytoma, a rare tumor of the adrenal gland that produces excess catecholamines (such as adrenaline and noradrenaline). Pheochromocytoma can cause symptoms such as high blood pressure, rapid heartbeat, and sweating, and can be difficult to diagnose. Measuring HIAA levels in the urine can help confirm the diagnosis of pheochromocytoma, especially when other diagnostic tests are inconclusive. HIAA is also sometimes used as a biomarker for other conditions, such as depression and certain types of cancer. However, more research is needed to fully understand the role of HIAA in these conditions.

Vesicular monoamine transport proteins (VMATs) are a family of proteins that play a critical role in the transport of monoamine neurotransmitters, such as dopamine, serotonin, and norepinephrine, into synaptic vesicles in neurons. These vesicles are small sacs that store neurotransmitters and release them into the synaptic cleft when an action potential reaches the presynaptic terminal. VMATs are responsible for loading these neurotransmitters into the vesicles, which is a critical step in the process of neurotransmitter release. There are two main types of VMATs: VMAT1 and VMAT2. VMAT1 is primarily found in the brain and is involved in the transport of dopamine, serotonin, and norepinephrine into presynaptic terminals. VMAT2 is found in the brain and peripheral tissues, and is primarily involved in the transport of dopamine and norepinephrine into presynaptic terminals. Disruptions in the function of VMATs have been implicated in a number of neurological and psychiatric disorders, including Parkinson's disease, Huntington's disease, and schizophrenia. For example, mutations in the VMAT2 gene have been associated with an increased risk of developing Parkinson's disease. Additionally, drugs that block VMATs, such as cocaine and amphetamines, can cause a range of side effects, including psychosis and addiction.

Vesicular biogenic amine transport proteins (VBATs) are a family of proteins that play a crucial role in the transport of biogenic amines, such as dopamine, serotonin, and norepinephrine, into synaptic vesicles in neurons. These vesicles are small sacs that store neurotransmitters and release them into the synaptic cleft when a nerve impulse reaches the end of a neuron. VBATs are responsible for loading these neurotransmitters into the vesicles, which is a critical step in the process of neurotransmitter release. They are found in a variety of organisms, including humans, and are encoded by several different genes. Mutations in these genes can lead to neurological disorders, such as Parkinson's disease and Huntington's disease. Overall, VBATs play a critical role in the regulation of neurotransmitter release and are an important target for the development of new treatments for neurological disorders.

Dopamine is a neurotransmitter that plays a crucial role in the brain's reward and pleasure centers. It is also involved in regulating movement, motivation, and emotional responses. In the medical field, dopamine is often used to treat conditions such as Parkinson's disease, which is characterized by a lack of dopamine in the brain. It can also be used to treat high blood pressure, as well as to manage symptoms of depression and schizophrenia. Dopamine is typically administered through injections or intravenous infusions, although it can also be taken orally in some cases.

Tyramine is a naturally occurring amino acid that is found in many foods, including cheese, chocolate, cured meats, and fermented foods. In the medical field, tyramine is known to increase the production of the neurotransmitter dopamine in the brain, which can lead to a range of symptoms, including headache, nausea, flushing, and rapid heartbeat. Tyramine is also a precursor to the neurotransmitter norepinephrine, which is involved in the body's "fight or flight" response. As a result, high levels of tyramine can cause symptoms such as anxiety, agitation, and increased heart rate. People with certain medical conditions, such as high blood pressure or a history of migraines, may need to avoid foods that are high in tyramine to prevent symptoms from occurring. In some cases, medications may be prescribed to help manage the effects of tyramine on the body.

Reserpine is a natural alkaloid that was originally isolated from the plant Rauvolfia serpentina, also known as the Indian snakeroot. It is a potent antagonist of the sympathetic nervous system, which means it blocks the effects of norepinephrine, a neurotransmitter that plays a key role in the body's "fight or flight" response. In the medical field, reserpine is primarily used as a medication to treat high blood pressure. It works by reducing the production of norepinephrine in the body, which can help lower blood pressure and reduce the risk of heart attack and stroke. Reserpine is also sometimes used to treat anxiety, depression, and other conditions that are thought to be related to imbalances in the sympathetic nervous system. Reserpine can cause a number of side effects, including dizziness, weakness, fatigue, and dry mouth. It can also cause more serious side effects, such as low blood pressure, rapid heart rate, and depression. As with any medication, it is important to talk to your doctor about the potential risks and benefits of taking reserpine, and to follow their instructions carefully.

Norepinephrine, also known as noradrenaline, is a neurotransmitter and hormone that plays a crucial role in the body's "fight or flight" response. It is produced by the adrenal glands and is also found in certain neurons in the brain and spinal cord. In the medical field, norepinephrine is often used as a medication to treat low blood pressure, shock, and heart failure. It works by constricting blood vessels and increasing heart rate, which helps to raise blood pressure and improve blood flow to vital organs. Norepinephrine is also used to treat certain types of depression, as it can help to increase feelings of alertness and energy. However, it is important to note that norepinephrine can have side effects, including rapid heartbeat, high blood pressure, and anxiety, and should only be used under the supervision of a healthcare professional.

3,4-Dihydroxyphenylacetic acid (DOPAC) is a metabolite of dopamine, a neurotransmitter that plays a crucial role in various brain functions such as movement, motivation, and reward. DOPAC is produced when dopamine is broken down by the enzyme monoamine oxidase (MAO) in the brain and other tissues. In the medical field, DOPAC is often measured in the cerebrospinal fluid (CSF) or blood as a biomarker of dopamine metabolism. Abnormal levels of DOPAC can be associated with various neurological and psychiatric disorders, including Parkinson's disease, Huntington's disease, schizophrenia, and depression. Additionally, DOPAC has been studied as a potential therapeutic target for these conditions, as modulating dopamine metabolism may help to improve symptoms and slow disease progression.

Fenclonine is a medication that is used to treat high blood pressure (hypertension). It is a type of medication called a beta-adrenergic receptor antagonist, which works by blocking the effects of certain hormones that can cause blood vessels to narrow and blood pressure to rise. Fenclonine is typically taken once or twice a day, and it is usually prescribed in combination with other medications to help lower blood pressure to a safe and healthy level. It is important to follow the instructions of your healthcare provider when taking fenclonine, as it can cause side effects such as dizziness, fatigue, and nausea.

Homovanillic acid (HVA) is a neurotransmitter metabolite that is produced by the breakdown of dopamine in the brain. It is a key marker of dopamine metabolism and is often used as a diagnostic tool in the evaluation of various neurological and psychiatric disorders. In the medical field, HVA is often measured in the cerebrospinal fluid (CSF) or in blood samples as a way to assess dopamine function and to diagnose conditions such as Parkinson's disease, Huntington's disease, and schizophrenia. It is also used to monitor the effectiveness of treatments for these conditions, such as dopamine replacement therapy. In addition to its use in the diagnosis and treatment of neurological and psychiatric disorders, HVA has also been studied in the context of addiction and substance abuse. It is believed that changes in HVA levels may play a role in the development and maintenance of addiction, and that measuring HVA levels in the brain may provide insight into the mechanisms underlying addiction and treatment response.

Methyltyrosines are a group of amino acids that have a methyl group (CH3) attached to the tyrosine residue. In the medical field, methyltyrosines are often used as markers for the presence of certain diseases or conditions, such as neurodegenerative disorders like Parkinson's disease or Alzheimer's disease. They are also used as markers for the presence of certain types of cancer, such as glioblastoma multiforme, a type of brain cancer. In addition, methyltyrosines have been shown to play a role in the regulation of various cellular processes, including cell growth and differentiation.

Monoamine oxidase (MAO) is an enzyme that is responsible for breaking down certain neurotransmitters in the brain, including serotonin, dopamine, and norepinephrine. These neurotransmitters play important roles in regulating mood, appetite, and other bodily functions. MAO inhibitors are a class of drugs that block the activity of this enzyme, allowing these neurotransmitters to remain in the brain for longer periods of time. This can lead to an increase in their effects and may be used to treat conditions such as depression and anxiety.

In the medical field, amines are organic compounds that contain a nitrogen atom bonded to one or more carbon atoms. They are often used as drugs, either as medications or as intermediates in the synthesis of other drugs. Amines can be classified into several categories based on their chemical structure and properties. Some common types of amines include primary amines, secondary amines, and tertiary amines. Primary amines have one nitrogen atom bonded to one hydrogen atom and two carbon atoms. Examples of primary amines include histamine, which is involved in allergic reactions, and dopamine, which plays a role in the regulation of movement and mood. Secondary amines have one nitrogen atom bonded to two hydrogen atoms and one carbon atom. Examples of secondary amines include epinephrine, which is used to treat severe allergic reactions and asthma, and norepinephrine, which is involved in the regulation of blood pressure and heart rate. Tertiary amines have one nitrogen atom bonded to three carbon atoms. Examples of tertiary amines include trimethoprim, which is used to treat bacterial infections, and procainamide, which is used to treat certain types of heart arrhythmias. Amines can also be classified based on their physical properties, such as their solubility in water and their ability to form salts with acids. Some amines are water-soluble and can be used as electrolytes in intravenous solutions, while others are insoluble and are used as local anesthetics.

Biogenic polyamines are a group of naturally occurring organic compounds that are synthesized in living organisms. They are primarily composed of three amino acids: ornithine, lysine, and arginine. Biogenic polyamines play important roles in various biological processes, including cell growth and division, DNA synthesis and repair, and regulation of gene expression. In the medical field, biogenic polyamines have been studied for their potential therapeutic applications. For example, some studies have suggested that biogenic polyamines may have anti-cancer properties, as they can inhibit the growth and proliferation of cancer cells. Additionally, biogenic polyamines have been shown to have anti-inflammatory effects, which may be useful in the treatment of various inflammatory diseases. Overall, biogenic polyamines are an important class of compounds that have a wide range of potential applications in the medical field.

Brain chemistry refers to the chemical processes that occur within the brain, including the production, release, and regulation of neurotransmitters, hormones, and other chemical messengers. These chemical processes play a critical role in regulating mood, behavior, cognition, and other aspects of brain function. In the medical field, brain chemistry is often studied in the context of neurological and psychiatric disorders, such as depression, anxiety, schizophrenia, and addiction. By understanding the underlying chemical imbalances or abnormalities in the brain, researchers and healthcare providers can develop more effective treatments for these conditions. Some common neurotransmitters and hormones involved in brain chemistry include dopamine, serotonin, norepinephrine, acetylcholine, and cortisol. Medications such as antidepressants, antipsychotics, and mood stabilizers often work by altering the levels of these chemicals in the brain to improve symptoms of various disorders.

ISBN 978-0-443-06911-6. Vianello R, Repič M, Mavri J (2012-10-25). "How are Biogenic Amines Metabolized by Monoamine Oxidases ... Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes that catalyze the oxidation of monoamines, employing oxygen to ... November 2006). "Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major ... Monoamine oxidases catalyze the oxidative deamination of monoamines. In the first part of reaction, cofactor FAD oxidase ...
The biogenic amine receptors include the monoamine receptors. Lawrence I. Gilbert (18 September 2009). Insect development: ... Biogenic amine receptor are a variety of neurotransmitter receptors that are sensitive to biogenic amine neurotransmitters. ... "Biogenic amines in neural signaling". Institute for Biological Information Processing. Archived from the original on 2006-07-15 ...
The biogenic amine hypothesis posits general dysregulation of monoamines underlies bipolar and affective disorders. The ... The role of monoamines in bipolar have been studied using neurotransmitter metabolites. Reduced concentration of homovanillic ... One more line of evidence that suggests a role of monoamines in bipolar is the process of antidepressant related affective ... Various hypotheses related to monoamines have been proposed. ... as indicating that more extensive perturbation in monoamine ...
Some prominent examples of biogenic monoamines include: Monoamine neurotransmitters Imidazoleamines Histamine - a substance ... Monoamine oxidase (MAO) breaks down biogenic amines and prevents excessive resorption. MAO inhibitors (MAOIs) are also used as ... Monoamine neurotransmitter Trace amine Santos, M.H.Silla (1996). "Biogenic amines: their importance in foods". International ... A biogenic amine is a biogenic substance with one or more amine groups. They are basic nitrogenous compounds formed mainly by ...
I. Effect on uptake and release of biogenic monoamines and on monoamine oxidase in the mouse brain". Acta Pharmacologica et ... para-Chloroamphetamine (PCA), also known as 4-chloroamphetamine (4-CA), is a substituted amphetamine and monoamine releaser ...
S. Tanaka and N. Takeda (1997). "Biogenic monoamines in the brain and the corpus cardiacum between albino and normal strains of ...
Sepiapterin is not detected by the regularly used methods applied in the investigation of biogenic monoamine metabolites in the ... The diagnosis of SR deficiency is based on the analysis of the pterins and biogenic amines found in the cerebrospinal fluid ( ... The pterin compound functions as a cofactor in enzyme catalysis and biogenic amines which include adrenaline, dopamine, and ... The Biogenic Amines. Available from: https://www.ncbi.nlm.nih.gov/books/NBK11035/. Echenne, B., Roubertie, A., Assmann, B., ...
"Modulation of Monoamine Transporters by Common Biogenic Amines via Trace Amine-Associated Receptor 1 and Monoamine ... Xie z, W. S. (2007). "Rhesus Monkey Trace Amine-Associated Receptor 1 Signaling: Enhancement by Monoamine Transporters and ... The presence of two Postsynaptic receptors with opposite abilities to regulate monoamine transporter function allows for ...
"Modulation of monoamine transporters by common biogenic amines via trace amine-associated receptor 1 and monoamine ... If monoamine metabolism is compromised by the use of monoamine oxidase inhibitors (MAOIs) and foods high in tyramine are ... Finberg JP, Gillman K (2011). "Selective inhibitors of monoamine oxidase type B and the "cheese effect"". Monoamine Oxidase and ... Tyramine is physiologically metabolized by monoamine oxidases (primarily MAO-A), FMO3, PNMT, DBH, and CYP2D6. Human monoamine ...
Monoamine reuptake inhibitor Monoamine receptor Monoamine oxidase Monoamine transporter Monoamine Hypothesis Biogenic amine ... Biogenic+monoamines at the U.S. National Library of Medicine Medical Subject Headings (MeSH) (CS1 French-language sources (fr ... which is a target of monoamine oxidase inhibitors, a class of antidepressants.[citation needed] Monoamine neurotransmitter ... All monoamines are derived from aromatic amino acids like phenylalanine, tyrosine, and tryptophan by the action of aromatic ...
... biogenic monoamines MeSH D02.092.211.215.311 - catecholamines MeSH D02.092.211.215.311.342 - dopamine MeSH D02.092.211.215. ... biogenic polyamines MeSH D02.092.211.415.261 - cadaverine MeSH D02.092.211.415.701 - putrescine MeSH D02.092.211.415.701.801 - ...
Based on the uptake of tritiated biogenic monoamine radiotracers it can be confirmed by observing the figures in the attached ...
Rothman RB, Partilla JS, Baumann MH, Lightfoot-Siordia C, Blough BE (2012). "Studies of the biogenic amine transporters. 14. ... A monoamine releasing agent (MRA), or simply monoamine releaser, is a drug that induces the release of a monoamine ... Once inside the presynaptic neuron, they may inhibit the reuptake of monoamine neurotransmitters through vesicular monoamine ... these transporters transport monoamines in reverse (i.e., they move monoamines from the neuronal cytoplasm into the synaptic ...
Monoamine oxidase inhibitors allow reuptake of biogenic amine neurotransmitters from the synapse, but inhibit an enzyme which ... Tricyclic antidepressants also block reuptake of biogenic amines from the synapse, but may primarily effect serotonin or ... Bender, KJ; Walker, SE (8 October 2012). "Irreversible Monoamine Oxidase Inhibitors Revisited". Psychiatric Times. Psychiatric ... and deprenyl inhibits monoamine oxidase (MAO)-B and thus increases dopamine levels. The serotonin created by the brain ...
It catalyzes the oxidative deamination of biogenic and xenobiotic amines and plays an important role in the catabolism of ... Monoamine oxidase A inhibitors have been typically used in the treatment of depression, and monoamine oxidase B inhibitors are ... Monoamine oxidase B, also known as MAOB, is an enzyme that in humans is encoded by the MAOB gene. The protein encoded by this ... "Entrez Gene: MAOB monoamine oxidase B". Cho HU, Kim S, Sim J, Yang S, An H, Nam MH, et al. (July 2021). "Redefining ...
VMAT2 is the CNS vesicular transporter for not only the biogenic amines DA, NE, EPI, 5-HT, and HIS, but likely also for the ... Vesicular monoamine transporter 2#Binding sites and ligands Fleckenstein AE, Volz TJ, Riddle EL, Gibb JW, Hanson GR (2007). " ... The vesicular monoamine transporter (VMAT) is a transport protein integrated into the membranes of synaptic vesicles of ... VMAT1 has a lower turnover number and a lower affinity for most monoamine substrates than VMAT2, which may be because of ...
Biogenic amines, Molecular neuroscience, Neurotransmitter transporters, Receptors, Signal transduction, Solute carrier family, ... Vesicular+Monoamine+Transporter+2 at the U.S. National Library of Medicine Medical Subject Headings (MeSH) (Articles with short ... Guo JT, Chen AQ, Kong Q, Zhu H, Ma CM, Qin C (2008). "Inhibition of vesicular monoamine transporter-2 activity in alpha- ... The solute carrier family 18 member 2 (SLC18A2) also known as vesicular monoamine transporter 2 (VMAT2) is a protein that in ...
Biogenic amines, Molecular neuroscience, Neurotransmitter transporters, Receptors, Signal transduction, Solute carrier family) ... The inward transport of the monoamine is coupled with the efflux of two protons per monoamine. The first proton is thought to ... Vesicular+Monoamine+Transporter+1 at the U.S. National Library of Medicine Medical Subject Headings (MeSH) (Articles with short ... Vesicular monoamine transporter 1 (VMAT1) also known as chromaffin granule amine transporter (CGAT) or solute carrier family 18 ...
The glycoproteins bind biogenic amines present in the CSF such as dopamine, serotonin or noradrenaline, thereby controlling the ... All findings obtained indicate that RF binds monoamines present in the ventricular CSF and then transports them along the ... The concentration of these monoamines in the CSF in Reissner's fiber-deprived animals was investigated, concluding that this ... In the absence of RF, the CSF concentration of monoamines increased sharply. Butler, Ann; William Hodos (Aug 23, 2005). ...
Cozzi NV, Sievert MK, Shulgin AT, Jacob P, Ruoho AE (September 1999). "Inhibition of plasma membrane monoamine transporters by ... Furthermore, they may cause release of biogenic amines from intracellular stores. It appears that N-ethylhexedrone has high ... These molecules are able to inhibit monoamine reuptake transporters producing a decreased clearance of the neurotransmitters ... substituted cathinones and benzofurans at biogenic amine transporters". Psychopharmacology. 236 (3): 939-952. doi:10.1007/ ...
... -mediated depletion of monoamine neurotransmitters in the synapses was cited as evidence that depletion of monoamine ... Reserpine was influential in promoting the thought of a biogenic amine hypothesis of depression. ... Yaffe D, Forrest LR, Schuldiner S (May 2018). "The ins and outs of vesicular monoamine transporters". The Journal of General ... Thus, it is the blockade of neuronal VMAT2 by reserpine that inhibits uptake and reduces stores of the monoamine ...
... vesicular monoamine transport proteins MeSH D12.776.157.530.562.750.625 - vesicular glutamate transport proteins MeSH D12.776. ... vesicular biogenic amine transport proteins MeSH D12.776.157.530.562.750.500.249 - vesicular acetylcholine transport proteins ... vesicular monoamine transport proteins MeSH D12.776.157.530.450.162.887.625 - vesicular glutamate transport proteins MeSH ... vesicular biogenic amine transport proteins MeSH D12.776.157.530.450.162.887.500.249 - vesicular acetylcholine transport ...
... vesicular monoamine transport proteins MeSH D12.776.543.585.562.750.625 - vesicular glutamate transport proteins MeSH D12.776. ... biogenic amine MeSH D12.776.543.750.720.300.300 - receptors, catecholamine MeSH D12.776.543.750.720.300.300.300 - receptors, ... vesicular monoamine transport proteins MeSH D12.776.543.585.450.162.887.625 - vesicular glutamate transport proteins MeSH ... vesicular biogenic amine transport proteins MeSH D12.776.543.585.562.750.500.249 - vesicular acetylcholine transport proteins ...
The term "neuro" refers to the dense core granules (DCGs), similar to the DCGs in the serotonergic neurons storing monoamines. ... uptake and decarboxylation to produce biogenic amines such as catecholamines and serotonin. Although this behavior was also ... The term "endocrine" refers to the synthesis and secretion of these monoamines. The neuroendocrine system includes endocrine ... and often producing biogenic amines and polypeptide hormones. ...
Similarly to PCP, RTI-4793-1 inhibits monoamine reuptake with moderate potency, but unlike PCP, has very low potency as an NMDA ... "Studies of the biogenic amine transporters. VI. Characterization of a novel cocaine binding site, identified with [125I]RTI-55 ... and it has been suggested that the site may be an allosteric/regulatory site of the monoamine transporters. RTI-4793-14 (HBMP ... and these interactions could potentially explain its monoamine reuptake inhibition as an alternative to the PCP site 2. Rothman ...
He is the discoverer of both monoamine oxidase (MAO) B inhibitors l-deprenyl (Selegiline) and rasagiline (Azilect) as anti- ... Biogenic Amines, Neuropsychobiology, Neurochemical Research; Brain Research, CNS Drug Review, Future Drugs, Drugs of Today, and ... He is a discoverer of the anti-Parkinson drugs selelgiline (l-deprenyl) and developer of monoamine oxidase B inhibitor ... Youdim, Moussa B H; Bakhle, Y S (2006). "Monoamine oxidase: isoforms and inhibitors in Parkinson's disease and depressive ...
... although it lacks monoamine transporter affinity and therefore has little effect in monoamine neurons of the central nervous ... Other biogenic amines are present in the central nervous system at very low concentrations in the order of 0.1-10 nm, ... Monoamine autoreceptors (e.g., D2 short, presynaptic α2, and presynaptic 5-HT1A) have the opposite effect of TAAR1, and ... In cells expressing both human TA1 and a monoamine transporter (DAT, SERT or NET) signalling via TA1 is enhanced [26,48,50-51 ...
Sánchez C, Hyttel J (1999). "Comparison of the effects of antidepressants and their metabolites on reuptake of biogenic amines ... "Pharmacological profile of antidepressants and related compounds at human monoamine transporters". European Journal of ... as it can lower the seizure threshold TCAs should not be used concomitantly or within 14 days of treatment with monoamine ...
Exogenous compounds in this family are degraded too rapidly by monoamine oxidase to be active at all but the highest doses. ... October 2003). "In vitro characterization of ephedrine-related stereoisomers at biogenic amine transporters and the receptorome ... Rothman RB, Baumann MH (2006). "Therapeutic potential of monoamine transporter substrates". Current Topics in Medicinal ...
It is substantially weaker in inhibiting the reuptake of and inducing the release of the monoamine neurotransmitters compared ... "Comparative actions of monomethoxyamphetamines on the release and uptake of biogenic amines in brain tissue". The Journal of ...
ISBN 978-0-443-06911-6. Vianello R, Repič M, Mavri J (2012-10-25). "How are Biogenic Amines Metabolized by Monoamine Oxidases ... Monoamine oxidases (MAO) (EC 1.4.3.4) are a family of enzymes that catalyze the oxidation of monoamines, employing oxygen to ... November 2006). "Elevated monoamine oxidase a levels in the brain: an explanation for the monoamine imbalance of major ... Monoamine oxidases catalyze the oxidative deamination of monoamines. In the first part of reaction, cofactor FAD oxidase ...
Biogenic Monoamines / metabolism * Brain / metabolism * Brain / pathology * Brain-Derived Neurotrophic Factor / genetics ...
Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. The net effect is ... 5] Long-term use can lead to a depletion of biogenic amine stores and a paradoxical reverse effect of the drug-a wash out. ... The degree to which an amphetamine can stimulate the receptors of these biogenic amines depends on the chemical substituents on ... Amphetamine compounds cause a general efflux of biogenic amines from neuronal synaptic terminals (indirect sympathomimetics). ...
Takeda N, Sugiyama K. (1993) Metabolism of biogenic monoamines in the ciliated protozoan, Tetrahymena pyriformis Comparative ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
Biogenic Amine Neurotransmitters. Biogenic Monoamines. D03 - Heterocyclic Compounds. Auxins. Indoleacetic Acids. D08 - Enzymes ...
1991, Adrenergic alpha-Antagonists/pharmacology, Adrenergic Antagonists, Analgesics/*pharmacology, Animals, Biogenic Monoamines ... Adrenergic alpha-Antagonists/pharmacology; Adrenergic Antagonists; Analgesics/*pharmacology; Animals; Biogenic Monoamines/ ...
Biogenic Amines [D02.092.211]. *Biogenic Monoamines [D02.092.211.215]. *Catecholamines [D02.092.211.215.311] ...
Biogenic Amines [D02.092.211]. *Biogenic Monoamines [D02.092.211.215]. *Catecholamines [D02.092.211.215.311] ...
... subjects provokes subjective and objective mental impairments tightly correlated with perturbation of biogenic monoamine ... Biogenic amines were measured with Chromsystems HPLC assay.. 2022. Change of Computed Tomography-Based Body Composition after ...
These are also sometimes called biogenic amines. Either monoamines or biogenic amines. The monoamines are organic molecules ... Nobody really knows what a good balance is and theres no way to measure your monoamine levels. You can get a monoamine blood ... Monoamine neurotransmitters, monoamines. Thats this whole row. Ive picked out five representative neurotransmitters for the ... Some of the monoamines, these three. Draw little stars next to these three, are also called by a different name and that name, ...
Serotonin (5-hydroxytryptamine [5-HT]) is a biogenic monoamine that plays various roles in metabolic homeostasis. It is well ... The monoamine transmitter theory suggests that neurotransmitters are involved in the mechanism of depression; however, the ... in Mouse Triptophan Hydroxylase 2 Gene in the Acute Effects of Ethanol on the c-fos Gene Expression and Metabolism of Biogenic ... Tph2 gene has a significant effect of acute ethanol administration on the c-fos expression pattern and metabolism of biogenic ...
Biogenic amines: Monoamines: 6-OHM. *Dopamine. *Epinephrine (adrenaline). *NAS (normelatonin). *Norepinephrine (noradrenaline) ...
Monoamines (a.k.a. Biogenic amines): dopamine (DA), norepinephrine (noradrenaline; NE, NA), epinephrine (adrenaline), histamine ... Small: Monoamine (Phe/Tyr). Dopamine. DA. Dopamine receptor. - Small: Monoamine (Phe/Tyr). Norepinephrine (noradrenaline). NE. ... Small: Monoamine (Phe/Tyr). Tyramine. - Small: Monoamine (Trp). Serotonin (5-hydroxytryptamine). 5-HT. Serotonin receptor, all ... Serotonin is a monoamine neurotransmitter. Most is produced by and found in the intestine (approximately 90%), and the ...
Hypotheses regarding depression have extended far beyond serotonin - indeed, far beyond biogenic amines (e.g., the monoamine ... Its primary target is glutamates NMDA receptor, not monoamine neurotransmitters. And its a sign that the research and ... Its also a sigma-1 receptor agonist, which modulates glutamate and monoamine neurotransmitter signaling. Yes, some serotonin ... Frankly, if Auvelitys primary target were monoamine neurotransmitters - specifically serotonin, norepinephrine, and dopamine ...
These effects of biogenic monoamines on the immune mediation were expressed through eicosanoids because the inhibitory effects ...
i] Petkov V.D., Stancheva S.L., Tocuschieva L., Petkov V.V. "Changes in brain biogenic monoamines induced by the nootropic ...
... blocker pindolol alone and in combination with the calcium antagonist verapamil on the level of biogenic monoamines in rat ... a potential antipsychotic on monoamine synthesis and release in rats. Society for Neuroscience Abstracts 22(1-3): 1188 ...
For example, it inhibits monoamine oxidase (the enzyme responsible for breaking down the biogenic amine neurotransmitters ...
Biogenic Monoamines - Serotonin * Biological Science Disciplines - Histocytochemistry * Cells - Neurons * Chemistry - ...
  • The phenylethylamine structure of amphetamines (see the image below) is similar to catecholaminergic, dopaminergic, and serotonergic agonists (biogenic amines), which may explain their actions. (medscape.com)
  • Amphetamine compounds cause a general efflux of biogenic amines from neuronal synaptic terminals (indirect sympathomimetics). (medscape.com)
  • They inhibit specific transporters responsible for reuptake of biogenic amines from the synaptic nerve ending and presynaptic vesicles. (medscape.com)
  • Biogenic amines were measured with Chromsystems HPLC assay. (chromsystems.com)
  • Therefore, the C1473G polymorphism in the Tph2 gene has a significant effect of acute ethanol administration on the c-fos expression pattern and metabolism of biogenic amines in the mouse brain. (bvsalud.org)
  • MAO (monoamine oxidase) A and B are key isoenzymes that degrade biogenic and dietary amines. (vidque.com)
  • These are also called biogenic amines. (studyread.com)
  • Pharmacologically, this action may potentiate or prolong neuronal activity since reuptake of these biogenic amines is important physiologically in terminating transmitting activity. (nih.gov)
  • Thermoregulatory effects of central injection of biogenic amines during arousal from hibernation. (kent.edu)
  • Interestingly, PEA's molecular mechanism of action differs from other biogenic amines, such as serotonin or dopamine. (performaxlabs.com)
  • Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. (medscape.com)
  • For example, it inhibits monoamine oxidase (the enzyme responsible for breaking down the biogenic amine neurotransmitters norepinephrine, serotonin, and dopamine) in the brain. (disruptedphysician.com)
  • Monoaminergic systems, i.e., the networks of neurons that use monoamine neurotransmitters, are involved in the regulation of processes such as emotion, arousal, and certain types of memory. (vidque.com)
  • Types of Neurotransmitters The monoamines include two subclasses of neurotransmitters, the catecholamines and the indolamines. (vidque.com)
  • Although traditionally it is believed that in mammalian spinal cord, monoamine neurotransmitters mainly originate from the brain, accumulating evidence indicates that especially when the spinal cord is injured, they can also be produced in the spinal cord. (vidque.com)
  • Which neurotransmitters are classified as monoamines? (vidque.com)
  • Monoamines refer to the particular neurotransmitters dopamine, noradrenaline and serotonin. (vidque.com)
  • Monoamine oxidase inhibitors (MAOIs) are an extremely strong class of antidepressants that treat depression by preventing the breakdown of the brain chemicals serotonin, dopamine, and norepinephrine. (vidque.com)
  • This leads in the alteration of the monoamine transporter functions, which results to inhibition of the reuptake of dopamine, serotonin, and norepinephrine. (performaxlabs.com)
  • Dividing them into amino acids , peptides , and monoamines is sufficient for some classification purposes. (wikidoc.org)
  • It should not be given concomitantly with monoamine oxidase inhibitors. (nih.gov)
  • Monoamine oxidase (MAO) is an enzyme involved in the degradation process for various monoamines released by neurons and glia cells, including DA, serotonin and norepinephrine (NE). (vidque.com)
  • [ 5 ] Long-term use can lead to a depletion of biogenic amine stores and a paradoxical reverse effect of the drug-a wash out. (medscape.com)
  • What receptors do monoamines bind to? (vidque.com)
  • Monoamines are neuromodulators that arise from the decarboxylation of large neutral and aromatic amino acids in brain tissue. (vidque.com)
  • All monoamines are derived from aromatic amino acids like phenylalanine, tyrosine, tryptophan, and the thyroid hormones by the action of aromatic amino acid decarboxylase enzyme s. (vidque.com)
  • All three MAOIs (isocarboxazid, phenelzine and tranylcypromine), available in the U.S. and used for the treatment of depression, are irreversible inhibitors of the enzyme monoamine oxidase. (vidque.com)
  • Where are monoamines produced in the brain? (vidque.com)
  • Phenylethylamine (PEA) is a naturally occurring monoamine in the brain that functions as a central nervous system (CNS) stimulant and neurotransmitter. (performaxlabs.com)
  • Hyperpyretic crises, severe convulsions, and deaths have occurred in patients receiving tricyclic antidepressant and monoamine oxidase inhibiting drugs simultaneously. (nih.gov)
  • It is not a monoamine oxidase inhibitor and it does not act primarily by stimulation of the central nervous system. (nih.gov)
  • Biogenic amine neurotransmitters metabolism is a multistep pathway with pterin and pyridoxal phosphate (vitamin B6) as cofactors. (nih.gov)
  • Amphetamines also inhibit monoamine oxidase, which degrades biogenic amine neurotransmitters intracellularly. (medscape.com)
  • MAO-A and MAO-B activities and levels of brain monoamines (serotonin (5-HT), dopamine (DA) and norepinephrine (NE)) and their deaminated metabolites were subsequently measured. (nih.gov)
  • Involved in the transport of biogenic monoamines, such as serotonin, from the cytoplasm into the secretory vesicles of neuroendocrine and endocrine cells. (nih.gov)
  • Deorphanisation of novel biogenic amine-gated ion channels identifies a new serotonin receptor for learning. (cam.ac.uk)
  • To be sure: what many psychiatrists in the 1980s and 1990s did promote was some version of the biogenic amine (or catecholamine) hypothesis of mood disorders, focusing mainly on the neurotransmitters norepinephrine and serotonin. (psychiatrictimes.com)
  • Serotonin (pronounced /ˌsɛrəˈtoʊnən/) (5-hydroxytryptamine, or 5-HT ) is a monoamine neurotransmitter synthesized in serotonergic neurons in the central nervous system (CNS) and enterochromaffin cells in the gastrointestinal tract of animals including humans. (gnosticserpent.com)
  • This study investigated the effects of acute and chronic (one daily i.p. injection for 14 days) treatments with the non-selective irreversible monoamine-oxidase (MAO) inhibitor phenelzine (10 and 30 mg/kg) on defensive behaviors of Swiss mice in the mouse defense test battery (MDTB) which has been designed for screening anxiolytic and anti-panic drugs. (nih.gov)
  • Marplan (isocarboxazid), a monoamine oxidase inhibitor, is available for oral administration in 10-mg tablets. (nih.gov)
  • Isocarboxazid is a non-selective hydrazine monoamine oxidase (MAO) inhibitor. (nih.gov)
  • It is not a monoamine oxidase inhibitor and it does not act primarily by stimulation of the central nervous system. (nih.gov)
  • When it is desired to replace a monoamine oxidase inhibitor with amitriptyline hydrochloride, a minimum of 14 days should be allowed to elapse after the former is discontinued. (nih.gov)
  • A defect in biogenic amine and cofactor metabolism and vesicular transporters result in a primary neurotransmitter disorders. (nih.gov)
  • This work aimed to study changes in cholinergic system focusing on acetylcholinesterase (ace-2), monoaminergic system focusing on vesicular monoamine transporter (VMAT, cat-1) expression, to address changes in antioxidant enzymatic systems, namely, the expression of superoxide dismutase (sod-3 and sod-4) and catalase (ctl-3), as well as worm reproduction and locomotion. (nih.gov)
  • The vesicular monoamine transporter acts to accumulate cytosolic monoamines into vesicles, using the proton gradient maintained across the vesicular membrane. (nih.gov)
  • Intestinal bacteria convert tyrosine into the biogenic and blood pressure-increasing amine tyramine, which is also found in high concentrations in cheese. (eliveragroup.com)
  • Hyperpyretic crises, severe convulsions, and deaths have occurred in patients receiving tricyclic antidepressant and monoamine oxidase inhibiting drugs simultaneously. (nih.gov)
  • [ 5 ] Long-term use can lead to a depletion of biogenic amine stores and a paradoxical reverse effect of the drug-a wash out. (medscape.com)
  • Included in this group are all natural monoamines formed by the enzymatic decarboxylation of natural amino acids. (nih.gov)
  • DLB subjects had the overall lowest monoamine and metabolite concentrations regarding 33 out of 41 significant monoaminergic group alterations. (biomedcentral.com)