Regulation of neuropeptide release
Regulation of neuropeptide release
复制标题
神经肽释放的调节
DOI：
10.1098/rspb.1980.0121
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发表时间：
1980
期刊：
影响因子：
--
通讯作者：
P. Emson
中科院分区：
文献类型：
--
作者：
L. Iversen;Chi;R. Gilbert;S. Hunt;P. Emson
去极化诱导的P物质、Met-和亮氨酸脑啡肽、生长抑素、神经紧张素、血管活性肠多肽和胆囊收缩素样物质从体外大鼠脑不同区域释放的证明，支持了这些和其他神经肽可能作为神经递质的假设。在每种情况下，肽的刺激诱发释放，而不是基础释放，依赖于钙离子在外部介质中的存在。刺激诱发的大鼠黑质神经末梢P物质释放可能受突触前γ-氨基丁酸（GABA）受体调控。含p物质感觉神经末梢可能存在突触前阿片受体，这可能解释了阿片在脊髓水平的镇痛作用，以及明胶质中存在脑啡肽神经元。辣椒素从脊髓神经末梢释放P物质，并可能损害其功能，而对棘上区P物质神经元无影响。讨论了从同一细胞中共同分泌肽和胺产物的可能性。
The demonstration of depolarization-induced release of substance P, Met- and Leu-enkephalin, somatostatin, neurotensin, vasoactive intestinal polypeptide and cholecystokinin-like material from various regions of rat brain in vitro supports the hypothesis that these and other neuropeptides may act as neurotransmitters. In each case the stimulusevoked release, but not the basal release, of peptide was dependent on the presence of calcium ions in the external medium. The stimulus-evoked release of substance P from nerve terminals in rat substantia nigra may be regulated by presynaptic γ-aminobutyric acid (GABA) receptors. The possible existence of presynaptic opiate receptors on substance P-containing sensory nerve terminals may offer an explanation for the analgesic effects of opiates at spinal cord level, and for the existence of enkephalin neurons in substantia gelatinosa. Capsaicin releases substance P from spinal cord nerve terminals and may impair their function, while having no effect on substance P neurons in supraspinal regions. The possibility of cosecretion of peptide and amine products from the same cells is discussed.