Weiner N
Fed Proc. 1979 Jul;38(8):2193-202.
Whereas extracellular calcium is absolutely required for neurotransmitter release consequent to stimulation of adrenergic and other neurons, a large number of substances are known to modify the amount of norepinephrine released per nerve impulse. In general, cyclic nucleotides, phosphodiesterase inhibitors, beta-adrenoceptor agonists, cholinergic nicotinic agonists, and angiotensin are able to enhance neurally mediated norepinephrine release, whereas alpha-adrenoreceptor agonists, cholinergic muscarinic agonists, prostaglandins of the E series, opiates, enkephalins, dopamine, and adenosine inhibit neurally mediated norepinephrine release. Although it has been proposed that cyclic AMP may enhance, and endogenous cyclic GMP may inhibit, neurotransmitter release, no consistent relationship between the effects of the several modulators of neurally mediated norepinephrine release and their effects on adenylate and guanylate cyclase is as yet apparent. The demonstration of whether such a relationship exists must await the development of techniques that will allow the measurement of cyclic nucleotide levels in the presynaptic adrenergic nerve terminal after exposure to the putative modulators of release and consequent to nerve stimulation.
尽管细胞外钙对于肾上腺素能神经元和其他神经元受刺激后释放神经递质是绝对必需的,但已知大量物质可改变每个神经冲动释放的去甲肾上腺素量。一般来说,环核苷酸、磷酸二酯酶抑制剂、β-肾上腺素能受体激动剂、胆碱能烟碱样激动剂和血管紧张素能够增强神经介导的去甲肾上腺素释放,而α-肾上腺素能受体激动剂、胆碱能毒蕈碱样激动剂、E系列前列腺素、阿片类药物、脑啡肽、多巴胺和腺苷则抑制神经介导的去甲肾上腺素释放。尽管有人提出环磷酸腺苷可能增强神经递质释放,而内源性环磷酸鸟苷可能抑制神经递质释放,但目前尚未发现几种神经介导的去甲肾上腺素释放调节剂的作用与其对腺苷酸环化酶和鸟苷酸环化酶的作用之间存在一致的关系。要证明这种关系是否存在,必须等待技术的发展,以便能够在暴露于假定的释放调节剂后以及神经刺激后测量突触前去甲肾上腺素能神经末梢中的环核苷酸水平。