[Feedback regulation of acetylcholine (ACh) on ion channel activity in snake motor nerve terminals].
In the vertebrate motor nerve terminals, the fact that the ACh release was affected by various activators and blockers of ACh receptors suggests the existence of several types of feedback regulation. The regulatory effect of ACh on the various ion channels in the snake motor nerve terminals was investigated by using subendothelial recording technique. (1) Suppression of IK(Ca). Similar to that of 3 mmol/L TEA, IK(Ca) could also be reversibly suppressed by 2 mmol/L ACh. (2) Regulatory effect on ICa. The time course of ICa in the presence of 30 mmol/L TEA was decreased by perfusion of 2 mmol/L ACh, an effect being more clear in high [Ca2+]o (7 mmol/L). The Ca2+ plateau, revealed by further addition of 3,4-DAP (300 mumol/L) to block all K+ channels, was also inhibited. These inhibitory effects could be reversed by 2 mmol/L atropine. It is likely that the inhibition of IK,f and IK(Ca) by ACh is to improve ACh release in normal condition, suggesting the presence of a positive feedback mechanism, while under circumstances in which ICa is increased, ACh may inhibit ICa so as to suppress the release itself as a result of negative feedback mechanism.
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Shanghai Institute of Physiology, Chinese Academy of Sciences.
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D000109:Acetylcholine / Q000502:physiology*; D000818:Animals; D015220:Calcium Channels / Q000378:metabolism; D005246:Feedback; D007473:Ion Channels / Q000378:metabolism*; D009411:Nerve Endings / Q000502:physiology*; D015221:Potassium Channels / Q000378:metabolism; D012911:Snakes / Q000502:physiology*
D015220:Calcium Channels; D007473:Ion Channels; D015221:Potassium Channels; D000109:Acetylcholine