摘要
目的 研究依托咪酯对大鼠大脑皮质突触体上不同钙通道的作用 ,探讨其抑制突触体内钙离子浓度升高可能涉及的钙离子通道亚型。方法 利用SD大鼠新鲜分离的大脑皮质突触体为研究对象 ,以KCl作为化学刺激剂去极化 ,采用荧光分光光度法测定依托咪酯 10 0mmol/L单用或与钙通道阻断剂合用的情况下对KCl诱发的突触体内钙离子浓度升高的影响。结果 P/Q型钙通道约占突触体钙内流的 5 0 % ,N型钙通道约占 2 0 % ,而L型钙通道不影响KCl诱发的突触体内钙离子浓度的升高。P/Q型钙通道阻断剂ω agatoxinIVA在单用或及与加入依托咪酯 10 0 μmol/L合用后对钙内流抑制作用没有差异 ,而L或N型钙通道阻断剂在加入依托咪酯后抑制钙内流作用增加。结论 P、N型钙通道在神经末梢去极化后钙离子内流中起主要作用。依托咪酯抑制高浓度KCl刺激引起的突触体内钙离子浓度升高可能与阻断P型 (可能还包括Q型 )钙离子通道有关。
Purpose To study the effects of etomidate on calcium channel subtypes on rat cerebrocortical synaptosomes. Methods By using freshly isolated SD rat cerebrocortical synaptosomes and KCl as chemical stimulant to depolarize,we investigated the effects of etomidate with or without calcium channel antagonists on KCl-induced increased intrasynaptosomal calcium concentrations with spectrofluorometer. Results The P-type (maybe including Q-type) calcium channel accounts for 50% calcium influx into synaptosomes,N-type for about 20%,while L-type didn't change KCl-induced increased intrasynaptosomal calcium concentrations.P/Q-type cal-cium channel antagonist ω-agatoxin IVA had no different effects on increased intrasynaptosomal calcium concentrations with or without 100 μmol/L etomidate,but for N- or L-type cal-cium channel antagonist,it had additional effects when with etomidate. Conclusions P-and N-type calcium channels played a primary role in calcium ion influx into nerve terminals when depolarization.And P/Q-type channels maybe involved in inhibitory effects of etomidate on KCl-induced increased intrasynaptosomal cal-cium concentrations.
出处
《复旦学报(医学版)》
CAS
CSCD
北大核心
2005年第2期216-218,228,共4页
Fudan University Journal of Medical Sciences