Intracellular injection of acetylcholine blocks various potassium conductances in vagal motoneurons.
Injection of acetylcholine into cholinergic neurons of the dorsal motor nucleus of the vagus induced membrane depolarization, an increase in input resistance, a decrease of early and late afterhyperpolarizations and a prolongation of the action potential. These effects were reversible and within 10-20 min almost complete recovery was always observed. Externally applied acetylcholine, even with doses as high as 15 mM, was not effective. Acetylcholine appeared to block voltage- and Ca2+-dependent K+ conductances. This block was manifested by the reduction of both the early and late afterhyperpolarizations and a decrease of the delayed rectification. The reversal potential for the conductance decrease was 15-30 mV negative to the resting potential. As a result of this blockade an increased Ca2+ current ensues, which is responsible for most of the prolongation of the action potential. The same responses were obtained after the injection of carbamylcholine, neostigmine and choline. However, unlike acetylcholine no sign of recovery was observed. In fact injection of neostigmine, carbamylcholine or neostigmine, together with acetylcholine, produced a delayed response which may reflect the accumulation of endogenous acetylcholine.
Yarom
Y
Y
Bracha
O
O
Werman
R
R
D000109:Acetylcholine / Q000494:pharmacology*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D002118:Calcium / Q000502:physiology*; D002217:Carbachol / Q000494:pharmacology; D002794:Choline / Q000494:pharmacology; D004553:Electric Conductivity; D006168:Guinea Pigs; D007473:Ion Channels / Q000187:drug effects*; D008526:Medulla Oblongata / Q000187:drug effects*; D009388:Neostigmine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D014630:Vagus Nerve / Q000187:drug effects*
D007473:Ion Channels; D009388:Neostigmine; D001285:Atropine; D002217:Carbachol; D002794:Choline; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium