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目的 在经新斯的明或 3,4 二氨基吡啶孵浴的大鼠膈肌标本上研究维拉帕米对终板电位的影响。方法 采用传统的微电极细胞内记录技术。结果 0 .2～ 5 .0 μmol·L- 1新斯的明或 1.0～ 4 .0 μmol·L- 13,4 二氨基吡啶 (3,4 DAP)均可以使膈肌终板电位产生持续性去极化。在正常台氏液中 ,维拉帕米 1、5、10、2 0 μmol·L- 1对单个和串终板电位以及小终板电位没有明显作用 ,但是 ,5～ 2 0 μmol·L- 1维拉帕米可以浓度依赖性方式抑制新斯的明或 3,4 DAP引起的持续性去极化。结论 成年大鼠膈神经末梢存在的L 型Ca2 +通道可以被新斯的明或 3,4 DAP所引起的突触间隙乙酰胆碱蓄积所激活 ,导致终板电位产生持续性去极化 ,而在正常生理状态下对突触传递不产生影响
OBJECTIVE: To investigate the effect of verapamil on the endplate potential of rat diaphragm specimens incubated with neostigmine or 3,4-diaminopyridine. Methods Using conventional microelectrode intracellular recording techniques. Results 0.02 ~ 5.0 μmol·L -1 neostigmine or 1.0-4.0 μmol·L-13,4 diaminopyridine (3,4 DAP) can make the diaphragmatic endplate potential to produce a sustained polarization. In normal Tyrode’s solution, 1,5,10,2 0 μmol·L-1 verapamil had no significant effect on single and series endplate potentials and small endplate potentials, however, 5-20 μmol·L- 1 Verapamil inhibits sustained depolarization caused by neostigmine or 3,4 DAP in a concentration-dependent manner. Conclusions L-type Ca2 + channels existing in the phrenic nerve terminals of adult rats can be activated by synaptic acetylcholine accumulation induced by neostigmine or 3,4 DAP, resulting in persistent depolarization of the terminal plate, whereas in normal Physiological state has no effect on synaptic transmission