钙离子对坐骨神经腓肠肌神经肌肉接头神经递质释放的作用.doc钙离子对坐骨神经腓肠肌神经肌肉接头神经递质释放的作用 作者:王宏李红芳陈方赵润平王成祥顾维刚韩杰 【摘要】目的探讨神经突触小体中神经递质量子释放的机制,并提出假设予以验证,从而明确Ca2+在这一过程中的作用。方法应用钙通道阻滞剂异搏定、蛋白激酶A的阻滞H89选择性作用于分离的蟾蜍坐骨神经腓肠肌标本上,通过观察腓肠肌的收缩程度,验证实验假设机制。结果 Ca2+组收缩曲线的振幅较正常组收缩曲线的振幅大(P<);异搏定组收缩曲线的振幅较正常组收缩曲线的振幅小(P<);H89组收缩曲线的振幅较正常组收缩曲线的振幅小(P<);Mg2+组收缩曲线的振幅较正常组收缩曲线的振幅小(P<)。结论 Ca2+促进了突触小体中神经递质的释放;异搏定、H89、Mg2+抑制了突触小体中神经递质的释放。 【关键词】 Ca2+; SNARE核心复合物; 神经递质释放机制; 蛋白激酶A; 突触 【Abstract】 Objective To explore the molecular mechanisms underlying neurotransmitter releasing from synaptic vesicles and confirm the exact effect in the process by proposing relative assumptions molecular mechanisms. Methods By using the verapamil (the antagonist against Ca2+ ion channel) and H89 (the antagonist against PKA) to the assumption in the consequence of observations on houch the muscle shrink after bEing stimulated. Results The amplitude of Ca2+ group's shrinkage curve plitude of the verapamil group is smaller than the one of control group's (P<). The amplitude of the H89 group aller than that of the control group (P<).The amplitude of the Mg2+ group aller than that of the control group (P<). Conclusion Ca2+ can stimulate neurotransmitter to release from synaptic vesicles. In the process of releasing, verapamil,H89 and Mg2+ play negative roles itter releasing. 【Key olecular mechanisms underlying neurotransmitter release;PKA