Castro E, Oset-Gasque M J, González M P
Instituto de Bioquimica (Centro mixto C.S.I.C.-U.C.M.), Facultad de Farmacia, Universidad Complutense, Madrid, Spain.
J Neurosci Res. 1989 Jul;23(3):290-6. doi: 10.1002/jnr.490230307.
GABA stimulates the basal catecholamine release from adrenal bovine chromaffin cells in a calcium-dependent manner. This release represents about 70% of that obtained by similar doses of nicotine under similar experimental conditions. This effect is mediated by GABAA receptor sites present in chromaffin cells, since it was mimicked by muscimol and reversed by bicuculline. In addition, GABA, through its GABAA receptors, increases the catecholamine release evoked by submaximal doses of nicotine, but it has no effect on nicotine-evoked secretion of catecholamines when nicotine was given at maximal doses. These results seem to indicate that both nicotine and GABA release catecholamines from the same intracellular pool. In contrast, baclofen, a GABAB receptor agonist, depressed both basal and nicotine-evoked catecholamine release; this result indicates that in addition to GABAA control of catecholamine secretion by chromaffin cells, there is a GABAB control of this function. These results support the existence of a dual regulation of catecholamine secretion by both the GABAA and GABAB receptors in a similar way as that proposed for muscarinic and nicotinic cholinergic receptors.
γ-氨基丁酸（GABA）以钙依赖的方式刺激肾上腺嗜铬细胞释放基础儿茶酚胺。在相似的实验条件下，这种释放量约为相似剂量尼古丁所引起释放量的70%。这种效应由嗜铬细胞中存在的GABAA受体介导，因为它可被蝇蕈醇模拟，并被荷包牡丹碱逆转。此外，GABA通过其GABAA受体，增强了亚最大剂量尼古丁诱发的儿茶酚胺释放，但当给予最大剂量尼古丁时，它对尼古丁诱发的儿茶酚胺分泌没有影响。这些结果似乎表明，尼古丁和GABA都从同一细胞内池释放儿茶酚胺。相反，GABAB受体激动剂巴氯芬抑制基础和尼古丁诱发的儿茶酚胺释放；这一结果表明，除了GABAA对嗜铬细胞儿茶酚胺分泌的调控外，还存在GABAB对该功能的调控。这些结果支持了GABAA和GABAB受体对儿茶酚胺分泌存在双重调控的观点，这与毒蕈碱和烟碱型胆碱能受体的调控方式类似。
