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.
|Original language||English (US)|
|Number of pages||7|
|Journal||Acta Physiologica Sinica|
|State||Published - Jan 1 1994|
- intracellular potential recording
- pancreatic B cells
ASJC Scopus subject areas