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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。
The effect of acetylcholine (ACh) on the islet B cell activity in mice was studied by recording the potential in cells and using extracellular micro-electrophoresis. Microelectrophoresis ACh depolarized the B cell membrane by 5-10 mV and increased the number of spiking potentials by 11-17 / 30s. This effect is glucose-dependent and is completely blocked by atropine, whereas pirenzepine suppresses 70% of the ACh effect. ACh membrane depolarization independent of extracellular Ca (2+), but can be tetrodotoxin (TTX) block; ACh increase the number of spangles depends on the effect of extracellular Ca2 +, but not by verapamil blocking. The results showed that glucose-dependent electrical activity of ACh-enhanced B cells was mediated by M receptor, mainly M1 subtype. ACh activated ion channels, including TTX-sensitive Na channel, Na + influx and membrane depolarization ; ACh may make verapamil is not sensitive to the opening of Ca channels, Ca2 influx occurs resulting in an increase in the number of spikes.