Segal M
Brain Res. 1982 Aug 19;246(1):77-87. doi: 10.1016/0006-8993(82)90144-5.
Responses of hippocampal pyramidal cells to topical application of acetylcholine (ACh) were measured in the in vitro hippocampal slice preparation. ACh but not cyclic GMP produced a short-latency hyperpolarization associated with a decrease in input resistance. This was followed by a long-latency but long duration depolarization associated in some cells with an increase in input resistance. This change in resistance followed the depolarization and outlasted it by 5--20 min, until complete recovery. During the depolarization there was a reduction in magnitude of EPSPs produced by activation of the Schaffer collateral excitatory afferents. The reversal potential for the hyperpolarization was about -95 mV, and it was blocked by 4-aminopyridine. The depolarization, but not the hyperpolarization was markedly attenuated in slices maintained in low (25 degrees C) temperature. The responses to ACh were blocked by atropine but not by D-tubocurarine. The hyperpolarization as well as the depolarization were present in slices treated with tetrodotoxin (TTX)., but were reduced in slices superfused with a low Ca2+-high Mg2+ medium, and in slices treated with Mn2+ and Co2+ ions. It is suggested that ACh causes a fast increase in gK+, followed by a long-lasting energy-dependent depolarization associated with action potential discharges, a decrease in conductance and a suppression of EPSPs.
在体外海马脑片标本中测量了海马锥体细胞对局部应用乙酰胆碱（ACh）的反应。ACh而非环鸟苷酸产生了与输入电阻降低相关的短潜伏期超极化。随后是一些细胞中与输入电阻增加相关的长潜伏期但持续时间长的去极化。这种电阻变化跟随去极化并比其持续5 - 20分钟，直至完全恢复。在去极化期间，由Schaffer侧支兴奋性传入激活产生的兴奋性突触后电位（EPSP）幅度减小。超极化的反转电位约为 - 95 mV，且被4 - 氨基吡啶阻断。在低温（25℃）下维持的脑片中，去极化而非超极化明显减弱。对ACh的反应被阿托品阻断，但不被筒箭毒碱阻断。超极化以及去极化在使用河豚毒素（TTX）处理的脑片中均存在，但在灌注低钙 - 高镁培养基的脑片以及用锰离子和钴离子处理的脑片中减弱。提示ACh导致钾离子电导快速增加，随后是与动作电位发放相关的持久的能量依赖性去极化、电导降低以及EPSP的抑制。
