前列腺素E1对青蛙运动神经自发乙酰胆碱释放的钙依赖性抑制作用。
Calcium-dependent inhibition by prostaglandin E1 of spontaneous acetylcholine release from frog motor nerve.
作者信息
Illés P, Vyskocil F
出版信息
Eur J Pharmacol. 1978 Apr 15;48(4):455-7. doi: 10.1016/0014-2999(78)90175-9.
PGE1 (10(-7) M) in the absence of Ca2+ or at low external Ca2+ concentrations (0.2-0.5 mM) depressed the frequency of miniature end-plate potentials (m.e.p.p.s) in frog sartorius muscle, but m.e.p.p. amplitudes were unchanged. Both an increase in Ca2+ concentration to 2 mM or a blockade of Ca2+ uptake into mitochondria by metabolic inhibitors (5 X 10(-5) M 2,4-dinitrophenol or 2 X 10(-5) M rotenone) prevented the inhibitory action of PGE1 on m.e.p.p. frequency. We suggest that PGE1 may inhibit acetylcholine release from motor nerve terminals by promoting the active uptake of Ca2+ by mitochondria, or by facilitating the efflux of Ca2+ from the axoplasm into the extracellular medium.
在无钙离子存在或细胞外钙离子浓度较低（0.2 - 0.5 mM）的情况下，前列腺素E1（10⁻⁷ M）可降低青蛙缝匠肌微小终板电位（m.e.p.p.s）的频率，但微小终板电位的幅度不变。将钙离子浓度提高到2 mM或用代谢抑制剂（5×10⁻⁵ M 2,4 - 二硝基苯酚或2×10⁻⁵ M鱼藤酮）阻断钙离子摄入线粒体，均可防止前列腺素E1对微小终板电位频率的抑制作用。我们认为，前列腺素E1可能通过促进线粒体对钙离子的主动摄取，或通过促进钙离子从轴浆外流到细胞外介质，从而抑制运动神经末梢乙酰胆碱的释放。
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