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青霉素诱导癫痫样活动的树突机制。

Dendritic mechanisms underlying penicillin-induced epileptiform activity.

作者信息

Wong R K, Prince D A

出版信息

Science. 1979 Jun 15;204(4398):1228-31. doi: 10.1126/science.451569.

Abstract

The action of penicillin on synaptically evoked dendritic activity was examined with the use of hippocampal slice preparations. Orthodormic activation of CA1 pyramidal neurons produced an excitatory-inhibitory postsynaptic potential sequence recorded intracellularly in the dendrites. Treatment with penicillin resulted in the appearance of spontaneous and synaptically evoked multipeaked field potentials and associated depolarization shifts and spike burst generation in CA1 cells. Intracellular recordings revealed that penicillin produced no detectable change in passive membrane properties of the postsynaptic dendrites. However, the inhibitory postsynaptic potential was suppressed by penicillin, resulting in the release of intrinsic dendritic burst firing during synaptic activation. These findings emphasize the role of normal patterns of dendritic burst generation in the production of intense neuronal discharge during penicillin-induced epileptiform activities.

摘要

利用海马脑片标本研究了青霉素对突触诱发的树突活动的作用。CA1锥体神经元的正向激活在树突内细胞内记录到兴奋性-抑制性突触后电位序列。青霉素处理导致CA1细胞中出现自发的和突触诱发的多峰场电位以及相关的去极化偏移和动作电位爆发。细胞内记录显示,青霉素对突触后树突的被动膜特性没有可检测到的影响。然而,青霉素抑制了抑制性突触后电位,导致在突触激活期间内在树突动作电位爆发的释放。这些发现强调了在青霉素诱导的癫痫样活动期间,正常的树突动作电位爆发模式在强烈神经元放电产生中的作用。

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