Biogenic amine receptor

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Biogenic amine receptors are "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 (also known as adrenaline and noradrenaline respectively), and dopamine, the indoleamine serotonin, the imidazolamine histamine, and compounds closely related to each of these."[1]

Biogenic amines are 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."[2]

Some biogenic amines, including dopamine, serotonin, and acetylcholine, are neurotransmitters.

Classification

Catecholamine receptors

Catecholamines are epinephrine, norepinephrine, dopamine. They are derived from the non-essential amino acid tyrosine which is found in casein in milk and cheese.

Catecholamine receptors are "cell surface proteins that bind catecholamines with high affinity and trigger intracellular changes which influence the behavior of cells. The catecholamine messengers epinephrine, norepinephrine, and dopamine are synthesized from tyrosine by a common biosynthetic pathway."[3]

Adrenergic receptors

For more information, see: Adrenergic receptor.


Dopamine receptors

For more information, see: Dopamine receptor.

Dopamine receptors are "cell-surface proteins that bind dopamine with high affinity and trigger intracellular changes influencing the behavior of cells."[4]

D1-like receptors

These receptors stimulate adenylate cyclase.[5]

D1 receptors
D5 receptors
D2-like receptors

These receptors inhibit adenylate cyclase.[6]

Dopamine D2 receptors

Agonists, such as metoclopramide, are used as antiemetics.

Antagonists, such as risperidone and haloperidol, are used to treat schizophrenia.[7]

Blockade of the D2 receptors, which may be predisposed by genetic polymorphisms of the allele, may cause neuroleptic malignant syndrome.[8]

D3 receptors

Agonists of D3, especially nonergot agonists such as pramipexole and ropinirole, may be used to treat Parkinonism and restless legs syndrome.[9]

D4 receptors

Histamine receptors

Histamine is an "amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter."[10]

Histamine receptors are "cell-surface proteins that bind histamine and trigger intracellular changes influencing the behavior of cells. Histamine receptors are widespread in the central nervous system and in peripheral tissues. Three types have been recognized and designated H1, H2, and H3. They differ in pharmacology, distribution, and mode of action."[11]

Histamine H1 receptors

Histamine H1 receptors "operate through the inositol phosphate/diacylglycerol second messenger system. Among the many responses mediated by these receptors are smooth muscle contraction, increased vascular permeability, hormone release, and cerebral glyconeogenesis."[12]

Antagonists, such as chorpheniramine, are used to treat allergic rhinitis.

Histamine H2 receptors

Histamine H2 receptors "act via G-proteins to stimulate adenylate cyclase. Among the many responses mediated by these receptors are gastric acid secretion, smooth muscle relaxation, inotropic and chronotropic effects on heart muscle, and inhibition of lymphocyte function."[13]

Antagonists, such as ranitidine, are used to treat gastrointestinal disorder such as peptic ulcer disease and gastroesophageal reflux disease that are due to hyperacidity.

Histamine H3 receptors

Histamine H3 receptors were "first recognized as inhibitory autoreceptors on histamine-containing nerve terminals and have since been shown to regulate the release of several neurotransmitters in the central and peripheral nervous systems.[14]

Serotonin receptors

Serotonin is 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."[15]

Serotonin receptors are "cell-surface proteins that bind serotonin and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action."[16]

Serotonin 5-HT1 receptors

Serotonin 5-HT1 receptors are in the central nervous system. Excess serotonin availability at the serotonin 1A receptor causes serotonin syndrome.

Agonists of serotonin 5-HT1D, such as sumatriptan, are used to treat migraine headaches.[17]

Serotonin 5-HT2 receptors

Antagonists, such as risperidone, are used to treat schizophrenia.

Agonists, such as fluoxetine, are used to treat depression and depression.

Agonists, such as lorcaserin, of the 5-HT2C receptor decreases appetite via the proopiomelanocortin system.[18] However, non-selective activation of the 5-HT2B receptors as well as the 5-HT2C receptors by fenfluramine and dexfenfluramine may damage heart valves via agonism of 5-HT2B receptors on valvular cells.

Serotonin 5-HT3 receptors

Serotonin 5-HT3 receptors stimulate gastrointestinal motility.

Antagonists, such as ondansetron, are used as an antiemetic for chemotherapy.[19] Antagonists, such as alosetron, are to treat diarrhea-predominant irritable bowel syndrome.

Serotonin 5-HT4 receptors

Serotonin 5-HT4 receptors stimulate gastrointestinal motility.

Agonists, such as tegaserod, are used to treat constipation-predominant irritable bowel syndrome.[20]

Amines in disease

Amine hypothesis and depression

Depletion of the amines serotonin and norepinephrine may contribute to depression.[21]

Dopamine hypothesis and schizophrenia

The dopamine hypothesis proposes that schizophrenia is in part due to excessive dopaminergic activity.[22]

References

  1. ↑ Anonymous (2024), Biogenic amine receptor (English). Medical Subject Headings. U.S. National Library of Medicine.
  2. ↑ Anonymous (2024), Biogenic Amines (English). Medical Subject Headings. U.S. National Library of Medicine.
  3. ↑ Anonymous (2024), Receptors, Catecholamine (English). Medical Subject Headings. U.S. National Library of Medicine.
  4. ↑ Anonymous (2024), Receptors, Dopamine (English). Medical Subject Headings. U.S. National Library of Medicine.
  5. ↑ Anonymous (2024), Receptors, Dopamine D1 (English). Medical Subject Headings. U.S. National Library of Medicine.
  6. ↑ Anonymous (2024), Receptors, Dopamine D2 (English). Medical Subject Headings. U.S. National Library of Medicine.
  7. ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 483. ISBN 0-8385-0598-8. 
  8. ↑ Kishida I, Kawanishi C, Furuno T, Kato D, Ishigami T, Kosaka K (2004). "Association in Japanese patients between neuroleptic malignant syndrome and functional polymorphisms of the dopamine D(2) receptor gene". Mol. Psychiatry 9 (3): 293-8. DOI:10.1038/sj.mp.4001422. PMID 15094790. Research Blogging.
  9. ↑ Baker WL, White CM, Coleman CI (2008). "Effect of nonergot dopamine agonists on symptoms of restless legs syndrome". Ann Fam Med 6 (3): 253–62. DOI:10.1370/afm.845. PMID 18474889. Research Blogging.
  10. ↑ Anonymous. Histamine. National Library of Medicine. Retrieved on 2008-01-16.
  11. ↑ Anonymous. Receptors, Histamine. National Library of Medicine. Retrieved on 2008-01-16.
  12. ↑ Anonymous. Receptors, Histamine H1. National Library of Medicine. Retrieved on 2008-01-16.
  13. ↑ Anonymous. Receptors, Histamine H2. National Library of Medicine. Retrieved on 2008-01-16.
  14. ↑ Anonymous. Receptors, Histamine H3. National Library of Medicine. Retrieved on 2008-01-16.
  15. ↑ Anonymous. Serotonin. National Library of Medicine. Retrieved on 2008-01-16.
  16. ↑ Anonymous. Receptors, Serotonin. National Library of Medicine. Retrieved on 2008-01-16.
  17. ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 280. ISBN 0-8385-0598-8. 
  18. ↑ Smith, Steven R.; Neil J. Weissman, Christen M. Anderson, Matilde Sanchez, Emil Chuang, Scott Stubbe, Harold Bays, William R. Shanahan, the Behavioral Modification and Lorcaserin for Overweight and Obesity Management (BLOOM) Study Group (2010-07-15). "Multicenter, Placebo-Controlled Trial of Lorcaserin for Weight Management". N Engl J Med 363 (3): 245-256. DOI:10.1056/NEJMoa0909809. Retrieved on 2010-07-15. Research Blogging.
  19. ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 279. ISBN 0-8385-0598-8. 
  20. ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 1069. ISBN 0-8385-0598-8. 
  21. ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 498. ISBN 0-8385-0598-8. 
  22. ↑ Katzung, Bertram G. (2001). Basic & clinical pharmacology. New York: Lange Medical Books/McGraw-Hill, 479. ISBN 0-8385-0598-8. 
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