大鼠海马CA1神经元群体反应的剥夺增强突触前和突触后机制。

IF 0.2 4区 医学 Q4 NEUROSCIENCES
V A Popov
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引用次数: 0

摘要

在体外实验中,研究了大鼠海马CA1神经元在停止少量(0.05 Hz)沙弗络刺激60 min后群体反应的剥夺增强(DeP)机制。研究表明,DeP的诱导有两种独立的机制:DeP初始阶段的突触前成分和DeP长期阶段的突触后成分。DeP长期阶段的机制与长期增强(LTP)蛋白磷酸化阶段的机制之间存在竞争性干扰。结果表明,非NMDA受体,而是嘌呤能P2受体参与了Ca(2+)依赖性的突触后DeP成分的诱导机制,并给出了包括DeP、长期抑制(LTD)和LTP区域在内的突触强度对突触使用/废用的共同依赖性曲线。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Pre- and Postsynaptic Mechanisms of the Deprivational Potentiation of Population Responses in Rat Hippocampal CA1 Neurons].

Mechanisms of the deprivational potentiation (DeP) of the population responses in rat hippocampal CA1 neurons after 60-min period of the cessation of rare (0.05 Hz) test stimulation of Schaffer collaterals was investigated in vitro. It has been demonstrated that two independent mechanisms are involved in DeP induction: presynaptic component in initial phase of DeP and postsynaptic one responsible for the long-term phase of DeP. The competitive interference between mechanisms of the long-term phase of DeP and the protein phosphorylation phase of long-term potentiation (LTP) was confirmed. It was shown that not NMDA receptors, but purinergic P2 receptors participate in Ca(2+) -dependent mechanism of induction of the postsynaptic component of DeP. The common curve of dependence of synaptic strength on synaptic use/disuse, including the DeP, long-term depression (LTD) and LTP areas, is presented.

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来源期刊
CiteScore
0.70
自引率
33.30%
发文量
9
审稿时长
6-12 weeks
期刊介绍: Information not localized
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