ETHANOL IN LOW-DOSES AUGMENTS CALCIUM-MEDIATED MECHANISMS MEASURED INTRACELLULARLY IN HIPPOCAMPAL-NEURONS
ETHANOL IN LOW-DOSES AUGMENTS CALCIUM-MEDIATED MECHANISMS MEASURED INTRACELLULARLY IN HIPPOCAMPAL-NEURONS
复制标题
DOI：
10.1126/science.7053581
复制
发表时间：
1982-01-01
期刊：
影响因子：
56.9
通讯作者：
DURAND, D
中科院分区：
文献类型：
--
作者：
CARLEN, PL;GUREVICH, N;DURAND, D
在体外对大鼠海马CA1细胞进行细胞内研究，检测了低剂量乙醇（5 - 20毫摩尔/升，相当于23 - 92毫克/100毫升）的电生理效应。当乙醇作用于相应的突触末梢区域时，抑制性和兴奋性突触后电位均增强。在突触后，乙醇作用于相应的突触末梢区域。在突触后，即使突触传递被阻断，乙醇也会引起膜电导增加的适度超极化。乙醇增强了在重复放电后或在河豚毒素存在下诱发钙峰后出现的超极化，但在无钙介质中不增强快速后超极化。乙醇似乎在突触前和突触后都增强了钙介导的机制。
The electrophysiological effects of ethanol in low doses (5-20 mmol/l on 23-92 mg/100 ml) were examined intracellularly in CA1 cells of rat hippocampus in vitro. Inhibitory and excitatory postsynaptic potentials were increased when ethanol was applied to the respective synaptic terminal regions. Postsynaptically, ethanol was applied to the respective synaptic terminal regions. Postsynaptically, ethanol caused a moderate hyperpolarization with increased membrane conductance, even when synaptic transmission was blocked. Ethanol augmented the hyperpolarization that followed repetitive firing or that followed the eliciting of Ca spikes in the presence of tetrodotoxin, but not the rapid afterhyperpolarization in Ca-free medium. Ethanol appears to augment Ca-mediated mechanisms both pre- and postsynaptically.