Gu C, Shi Y L
Shanghai Institute of Physiology, Chinese Academy of Sciences.
Sheng Li Xue Bao. 1996 Dec;48(6):529-35.
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.
在脊椎动物运动神经末梢，乙酰胆碱（ACh）的释放受到ACh受体的各种激活剂和阻滞剂影响这一事实表明存在几种类型的反馈调节。利用内皮细胞下记录技术研究了ACh对蛇运动神经末梢中各种离子通道的调节作用。（1）IK（Ca）的抑制。与3 mmol/L四乙铵（TEA）类似，2 mmol/L ACh也能可逆地抑制IK（Ca）。（2）对ICa的调节作用。在存在30 mmol/L TEA的情况下，通过灌注2 mmol/L ACh可使ICa的时程缩短，在高细胞外钙离子浓度（[Ca2+]o，7 mmol/L）时这种作用更明显。通过进一步添加3,4-二氨基吡啶（3,4-DAP，300 μmol/L）阻断所有钾离子通道所揭示的钙离子平台也受到抑制。这些抑制作用可被2 mmol/L阿托品逆转。ACh对IK,f和IK（Ca）的抑制作用可能是为了在正常情况下促进ACh的释放，提示存在正反馈机制，而在ICa增加的情况下，ACh可能抑制ICa，从而通过负反馈机制抑制其自身的释放。
