Monoaminergic activity enhancer

Monoaminergic activity enhancer
Drug class
Selegiline, the prototypical MAE.
Class identifiers
SynonymsMAE; Monoamine activity enhancer; Catecholaminergic activity enhancer; Catecholamine activity enhancer; CAE; Dopaminergic activity enhancer; Dopamine activity enhancer; DAE; Serotonergic activity enhancer; Serotonin activity enhancer; SAE; Catecholaminergic/serotonergic activity enhancer; CAE/SAE
UseDepression, Parkinson's disease, other conditions
Mode of actionEnhancement of the action potential-mediated release of monoamine neurotransmitters
Mechanism of actionPossibly TAAR1 agonism[1][2][3][4]
Chemical classPhenethylamines, tryptamines, benzofurans, others
Legal status
In Wikidata

Monoaminergic activity enhancers (MAE), also known as catecholaminergic/serotonergic activity enhancers (CAE/SAE), are a class of drugs that enhance the action potential-evoked release of monoamine neurotransmitters in the nervous system.[5] MAEs are distinct from monoamine releasing agents (MRAs) like amphetamine and fenfluramine in that they do not induce the release of monoamines from synaptic vesicles but rather potentiate only nerve impulse propagation-mediated monoamine release.[1][6] That is, MAEs increase the amounts of monoamine neurotransmitters released by neurons per electrical impulse.[1][6]

MAEs have been shown to significantly enhance nerve impulse-mediated dopamine release in the striatum, substantia nigra, and olfactory tubercle; norepinephrine release from the locus coeruleus; and/or serotonin release from the raphe nucleus in rodent studies.[7] Some MAEs are selective for effects on some of these neurotransmitters but not on others.[1][7] The maximal impacts of MAEs on brain monoamine levels are more modest than with monoamine releasing agents like amphetamine and monoamine reuptake inhibitors like methylphenidate.[7][8] MAEs have a peculiar and characteristic bimodal concentration–response relationship, with two bell-shaped curves of MAE activity across tested concentration ranges.[1][9][7][4][10] Hence, there is a restricted concentration range for optimal pharmacodynamic activity.[9]

Endogenous MAEs include certain trace amines like β-phenylethylamine and tryptamine, while synthetic MAEs include certain phenethylamine and tryptamine derivatives like selegiline, phenylpropylaminopentane (PPAP), benzofuranylpropylaminopentane (BPAP), and indolylpropylaminopentane (IPAP).[1][7][3] Although this was originally not known, the actions of MAEs may be mediated by agonism of the trace amine-associated receptor 1 (TAAR1).[1][2][3][4] Antagonists of MAEs, like EPPTB (a known TAAR1 antagonist), 3-F-BPAP, and rasagiline, have been identified.[3][4][7]

  1. ^ a b c d e f g Shimazu, Seiichiro; Miklya, Ildikó (2004-05-01). "Pharmacological studies with endogenous enhancer substances: β-phenylethylamine, tryptamine, and their synthetic derivatives". Progress in Neuro-Psychopharmacology and Biological Psychiatry. 28 (3): 421–427. doi:10.1016/j.pnpbp.2003.11.016. ISSN 0278-5846. PMID 15093948. S2CID 37564231.
  2. ^ a b Cite error: The named reference Berry2007 was invoked but never defined (see the help page).
  3. ^ a b c d Cite error: The named reference HarsingKnollMiklya2022 was invoked but never defined (see the help page).
  4. ^ a b c d Cite error: The named reference HarsingTimarMiklya2023 was invoked but never defined (see the help page).
  5. ^ Cite error: The named reference Knoll2001 was invoked but never defined (see the help page).
  6. ^ a b Bhattacharjee, Monojit; Perumal, Ekambaram (2019-03-01). "Potential plant-derived catecholaminergic activity enhancers for neuropharmacological approaches: A review". Phytomedicine. 55: 148–164. doi:10.1016/j.phymed.2018.07.010. ISSN 0944-7113. PMID 30668425. S2CID 58948967.
  7. ^ a b c d e f Knoll J (2005). "Enhancer Regulation: A Neurochemical Approach to the Innate and Acquired Drives". The Brain and Its Self: A Neurochemical Concept of the Innate and Acquired Drives. Berlin/Heidelberg: Springer-Verlag. pp. 25–94. doi:10.1007/3-540-27434-0_4. ISBN 978-3-540-23969-7.
  8. ^ Cite error: The named reference HealSmithKulkarni2008 was invoked but never defined (see the help page).
  9. ^ a b Knoll J (August 2003). "Enhancer regulation/endogenous and synthetic enhancer compounds: a neurochemical concept of the innate and acquired drives". Neurochem Res. 28 (8): 1275–1297. doi:10.1023/a:1024224311289. PMID 12834268.
  10. ^ Knoll J, Miklya I, Knoll B, Yasusa T, Shimazu S, Yoneda F (September 2002). "1-(Benzofuran-2-yl)-2-(3,3,3-trifluoropropyl)aminopentane HCl, 3-F-BPAP, antagonizes the enhancer effect of (-)-BPAP in the shuttle box and leaves the effect of (-)-deprenyl unchanged". Life Sci. 71 (17): 1975–84. doi:10.1016/s0024-3205(02)01968-9. PMID 12175892.
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