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由研究乙酰胆碱受体激动剂和阻断剂的作用提出，在脊椎动物运动神经末梢存在着对乙酰胆碱（ＡＣｈ）释放的反馈调节。神经末梢的离子通道在递质释放中有重要作用。本文是利用周膜下记录技术，研究ＡＣｈ对蛇运动神经末梢离子通道调节作用的报告。（１）２ｍｍｏｌ／ＬＡＣｈ明显抑制依钙Ｋ＋流（ＩＫ，Ｃａ），此效应与３ｍｍｏｌ／ＬＴＥＡ的相似。由于ｎＡＣｈＲ激动剂尼古丁（２ｍｍｏｌ／Ｌ）不影响ＩＫ，ｆ和ＩＫ，Ｃａ，阿托品对ＡＣｈ抑制ＩＫ，ｆ和ＩＫ，Ｃａ的作用无影响，提示上述作用是由阿托品不敏感的ｍＡＣｈＲ介导的。（２）ＡＣｈ对钙流（ＩＣａ）的调控。由３０ｍｍｏｌ／ＬＴＥＡ暴露的Ｉｃａ在加入２ｍｍｏｌ／ＬＡＣｈ后时程缩短，升高溶液中Ｃａ２＋浓度（至７ｍｍｏｌ／Ｌ）后此效应更加明显，作用是可逆的。对同时加入ＴＥＡ（３０ｍｍｏｌ／Ｌ）和３，４－ＤＡＰ（３００μｍｏｌ／Ｌ）阻断全部Ｋ＋通道所暴露的Ｃａ平台，ＡＣｈ有明显抑制作用。２ｍｍｏｌ／Ｌ的阿托品可部分逆转这种效应。由这些结果推测，在正常情况下ＡＣｈ通过抑制ＩＫ，ｆ和ＩＫ，Ｃａ促进ＡＣｈ释放，实行正反馈调节；而在Ｉｃａ异常增大时，ＡＣｈ通过抑制ＩＣａ，抑制ＡＣｈ释放，实行负反馈调节。
It has been suggested by studying the action of acetylcholine receptor agonists and blockers that feedback regulation of acetylcholine (ACh) release exists at the motor nerve endings of vertebrates. The ion channels of nerve endings play an important role in the release of neurotransmitters. This article is the use of recording techniques under the peritubular membrane to study ACh snake motor nerve endings ion channel regulation of the report. (1) 2mmol / LACh obviously inhibited the calcium-dependent K + flux (IK, Ca), and the effect was similar to that of 3mmol / LTEA. As nAChR agonist nicotine (2 mmol / L) did not affect IK, f and IK, Ca, atropine had no effect on ACh inhibition of IK, f and IK, Ca, suggesting that the above effects are mediated by atropine insensitive mAChR. (2) ACh regulation of calcium flow (ICa). The Ica exposed by 30mmol / L of LTE was shortened after adding 2mmol / LACh, and the effect was more obvious when the Ca2 + concentration in the solution was increased (up to 7mmol / L), and the effect was reversible. ACh was significantly inhibited by simultaneous addition of TEA (30 mmol / L) and 3,4-DAP (300 μmol / L) to block Ca channels exposed by all K + channels. Atropine at 2 mmol / L partially reversed this effect. From these results, we hypothesize that under normal conditions, ACh promotes ACh release by inhibiting IK, f and IK, Ca, and positive feedback regulation. When Ica is abnormally increased, ACh exerts negative feedback regulation by inhibiting ICa and inhibiting ACh release.