Analysis of the acetylcholine action on the electrical activities of pancreatic islet B-cells in mice

Intracellular potential recording and extracellular microiontophoretic techniques were 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 (11-17/30 s) by the ACh microinotophoresis. These effects were dependent on glucose and completely blocked by atropine. However, pirenzepine could attenuate the electrical activity by approximately 70%. The ACh-induced membrane depolarization was Ca²⁺-independent and blocked by TTX. But the effect of ACh on spikes was Ca²⁺-dependent and not blocked by verapamil. The results showed that ACh action in the enhancement of glucose-dependent electrical activities of B-cell were mediated by muscarinic receptor, mainly by subtype M₁. Then TTX-sensitive Na channel and verapamil-insensitive Ca channel were activated by M₁ receptors. Na⁺ influx resulted in membrane depolarization and Ca²⁺ influx enhanced spike discharges.