乙酰胆碱对小鼠胰岛B细胞电活动作用的分析  

ANALYSIS OF THE ACETYLCHOLINE ACTIONON THE ELECTRICAL ACTIVITIES OFPANCREATIC ISLET B-CELLS IN MICE

作　　者：陶锋[1] 苏清芬[1] 张镜如[1] 

机构地区：[1]上海医科大学生理学教研室

出　　处：《生理学报》1994年第2期105-111,共7页Acta Physiologica Sinica

基　　金：国家自然科学基金

摘　　要：用细胞内电位记录和细胞外微电泳技术，研究乙酰胆碱（ＡＣｈ）对小鼠胰岛Ｂ细胞电活动的作用。微电泳ＡＣｈ使Ｂ细胞膜去极化５—１０ｍＶ和锋电位发放数增加１１—１７／３０ｓ。这种效应具有葡萄糖依赖性，并被阿托品完全阻断，而哌仑西平可阻抑ＡＣｈ效应的７０％。ＡＣｈ的膜去极化作用不依赖于细胞外Ｃａ（２＋），而可被河豚毒（ＴＴＸ）阻断；ＡＣｈ增加锋电位数的效应依赖于细胞外Ｃａ２＋，但不被异搏定阻断。结果表明：ＡＣｈ增强Ｂ细胞葡萄糖依赖的电活动是由Ｍ受体介导的，主要为Ｍ１亚型；ＡＣｈ能激活离子通道，其中有ＴＴＸ敏感的Ｎａ通道，发生Ｎａ＋内流而使膜去极化；ＡＣｈ可能使对异搏定不敏感的Ｃａ通道开放，发生Ｃａ２＋内流而导致锋电位数增多。Intracellular potential recording and extracellular microiontophoretic techniqueswere used to study the acetylcholine(ACh)action on the electrical activities of pancreatic islet B-cells in mice.The B cell membrane potential was decreased (5-10 mV)and the spikes were increased(if-17/30s)by the ACh microinotophoresis.These effects were dependenton glucose and completely blocked by atropine.However,pirenzepine could attenuatethe electrical activity by approximately 70%.The ACh-induced membrane depolarization was Ca2+-independent and blocked by TTX.But the effect of ACh on spikes wasCa2+-dependent and not blocked by verapamil.The results showed that ACh action in the enhancment of glucose-dependent electri-cal activities of B-cell were mediated by muscarinic receptor,mainly by subtype M1.Then TTX-sensitive Na channel and verapamil-insensitive Ca channel were activatedby M1 receptors.Na+ influx resulted in membrane depolarization and Ca2+ influx enhanced spike discharges.

关 键 词：胰岛 B细胞 乙酰胆碱 电活动 

分 类 号：R335.6[医药卫生—人体生理学]