[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 Ca(2+)-independent and blocked by TTX. But the effect of ACh on spikes was Ca(2+)-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.
Department of Physiology, Shanghai Medical University.
F
F
Tao
Q F
QF
Su
J R
JR
Zhang
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D002118:Calcium / Q000378:metabolism; D005260:Female; D007478:Iontophoresis; D007515:Islets of Langerhans / Q000166:cytology / Q000502:physiology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051379:Mice; D011976:Receptors, Muscarinic / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D011976:Receptors, Muscarinic; D013779:Tetrodotoxin; D000109:Acetylcholine; D002118:Calcium