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突触可塑性:长时程增强和长时程抑制

Synaptic plasticity: LTP and LTD.

作者信息

Bear M F, Malenka R C

机构信息

Department of Neuroscience, Brown University, Providence, Rhode Island 02912.

出版信息

Curr Opin Neurobiol. 1994 Jun;4(3):389-99. doi: 10.1016/0959-4388(94)90101-5.

Abstract

Long-term potentiation (LTP) is a synaptic enhancement that follows brief, high-frequency electrical stimulation in the hippocampus and neocortex. Recent evidence suggests that induction of LTP may require, in addition to postsynaptic Ca2+ entry, activation of metabotropic glutamate receptors and the generation of diffusible intercellular messengers. A new form of synaptic plasticity, homosynaptic long-term depression (LTD) has also recently been documented, which, like LTP, requires Ca2+ entry through the NMDA receptor. Current work suggests that this LTD is a reversal of LTP, and vice versa, and that the mechanisms of LTP and LTD may converge at the level of specific phosphoproteins.

摘要

长时程增强(LTP)是一种突触增强现象,它在海马体和新皮层中短暂的高频电刺激后出现。最近的证据表明,除了突触后Ca2+内流外,LTP的诱导可能还需要代谢型谷氨酸受体的激活以及可扩散细胞间信使的产生。一种新的突触可塑性形式,即同突触长时程抑制(LTD),最近也有文献记载,它与LTP一样,需要通过NMDA受体的Ca2+内流。目前的研究表明,这种LTD是LTP的逆转,反之亦然,并且LTP和LTD的机制可能在特定磷酸化蛋白水平上趋同。

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