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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-1 3,4-二氨基吡啶(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、20 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, 5～20 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.“,”AIM To study the effects of verapamil on end-plate potentials(EPPs) in isolated non-uniform stretched muscle preparation(INSMP) of rat diaphragms pretreated with neostigmine or 3,4-diaminopyridine(3,4-DAP). METHODS Using conventional intracellular microelectrode recording technique. RESULTS A sustained depolarization could be induced at the end-plate area pre-incubated with 0.2－5.0 μmol·L-1 neostigmine or 1.0－4.0 mmol·L-1 3,4-DAP. In normal Tyrode solution, verapamil at a concentration of 1, 5, 10 or 20 μmol·L-1 had no significant effect on evoked endplate potentials and miniature endplate potentials. However, the sustained depolarization due to neostigmine or 3,4-DAP could be antagonized by verapamil at 5－20 μmol·L-1 and the duration of the depolarization was shortened in a concentration-dependent manner. CONCLUSIONL-type calcium ion channels can be activated by accumulated acetylcholine in the synaptic cleft and may be involved in producing sustained depolarization, while they play no role in transmitter release under normal physiological conditions.