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在突触传递过程中,动作电位引起神经递质释放的关键性环节,是去极化作用促进Ca~(++)进入神经末梢,触发神经递质的释放,这一点已得到公认。但迄今为止,去极化作用是通过哪一环节或途径促进Ca~(++)进入神经末梢?这一细节尚不清楚。已有资料指出,Ca~(++)内流和神经递质释放可能与突触小体膜的磷酯酸(phosphatidate,PA)的含量变化有关。电刺激突触小体可使~(32)P掺入PA的量增多,同时Ca~(++)转运增加,故推测PA可能与Ca~(++)转运有关。Harris等为了证明PA在去极化和Ca~(++)内流之间是否有可能起着一个耦联剂的作用,将PA或K~+分别加入大鼠脑纹状体的突触小体制备里,观察实触小体对Ca~(++)摄取的影响。
During the process of synaptic transmission, the pivotal part of action potential to cause the release of neurotransmitter is depolarization to promote Ca ~ (++) into the nerve endings and trigger the release of neurotransmitter. However, to date, what is the mechanism by which depolarization promotes Ca ~ (++) entry into nerve endings? It has been reported that Ca ~ (++) influx and neurotransmitter release may be related to the changes of phosphatidate (PA) content in synaptosome membrane. Electrical stimulation of synaptosomes could increase the amount of ~ (32) P incorporated into PA and increase the transport of Ca ~ (++), suggesting that PA may be involved in Ca ~ (++) transport. Harris et al. To demonstrate whether PA may play a role as a coupling agent between depolarization and Ca ~ (++) influx, PA or K ~ + was added to the synaptic small In vivo preparation, observe the influence of real body on Ca ~ (++) uptake.