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Monoamine Oxidase (MAO)‐A but Not MAO‐B Inhibitors Potentiate Tyramine‐Induced Catecholamine Release from PC12 Cells
Author(s) -
Youdim Moussa B. H.
Publication year - 1990
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1990.tb01888.x
Subject(s) - tyramine , clorgyline , catecholamine , monoamine oxidase , chemistry , monoamine oxidase a , monoamine neurotransmitter , monoamine oxidase b , pharmacology , endocrinology , serotonin , medicine , biochemistry , biology , enzyme , receptor
The previous report that PC12 (pheochromocytoma) cells have a K + ‐induced, as well as a tyramine‐induced, catecholamine release mechanism has been confirmed. Selective monoamine oxidase (MAO)‐A (clorgyline and moclobemide) and not MAO‐B inhibitors ( l ‐deprenyl, AGN 1135, and Ro 16–6491) potentiate the catecholamine‐releasing action of tyramine significantly more than that of K + . The potentiation of tyramine‐induced [ 3 H]noradrenaline release from PC 12 cells by MAO‐A inhibitors has been linked to the presence of MAO‐A in these cells, for which tyramine and noradrenaline are substrates. In the above respects, it is the PC 12 cell that resembles more closely the peripheral adrenergic neuron, rather than the chromaffin cell, which is endowed with MAO‐B and lacks the tyramine‐releasable pool of catecholamines.