维拉帕米对新斯的明或3,4-二氨基吡啶引起的大鼠膈肌持续性去极化的作用(英文)  

Effects of verapamil on the sustained depolarization of rat diaphragm myocyte pretreated with neostigmine or 3,4-diaminopyridine

作　　者：李立君[1] 刘传缋[1] 

机构地区：[1]军事医学科学院毒物药物研究所,北京100850

出　　处：《中国药理学与毒理学杂志》2002年第1期1-7,共7页Chinese Journal of Pharmacology and Toxicology

摘　　要：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 。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. CONCLUSION L 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.

关 键 词：神经肌接头 钙通道 终板电位 持续性去极化 维拉帕米 新斯的明 3 4-二氨基吡啶 

分 类 号：R965[医药卫生—药理学]