Youdim M B
Rappaport Family Research Institute and Department of Pharmacology, Faculty of Medicine, Technion, Haifa, Israel.
J Neurochem. 1990 Feb;54(2):411-4. doi: 10.1111/j.1471-4159.1990.tb01888.x.
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 [3H]noradrenaline release from PC12 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 PC12 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.
先前关于PC12(嗜铬细胞瘤)细胞具有钾离子诱导以及酪胺诱导的儿茶酚胺释放机制的报道已得到证实。选择性单胺氧化酶(MAO)-A抑制剂(氯吉兰和吗氯贝胺)而非MAO-B抑制剂(左旋司来吉兰、AGN 1135和Ro 16-6491)对酪胺的儿茶酚胺释放作用的增强明显超过对钾离子的增强作用。MAO-A抑制剂增强酪胺诱导的PC12细胞[3H]去甲肾上腺素释放,这与这些细胞中存在MAO-A有关,酪胺和去甲肾上腺素是MAO-A的底物。在上述方面,PC12细胞比嗜铬细胞更类似于外周肾上腺素能神经元,嗜铬细胞含有MAO-B且缺乏可被酪胺释放的儿茶酚胺池。