Nicotine compensates for the loss of cholinergic function to enhance long-term potentiation induction

被引：34

作者：

Yamazaki, Y ^{[1
]}

Hamaue, N ^{[1
]}

Sumikawa, K ^{[1
]}

机构：

[1] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA

来源：

BRAIN RESEARCH | 2002年 / 946卷 / 01期

关键词：

nicotinic acetylcholine receptor; nicotine; N-methyl-D-aspartate receptor; long-term potentiation; synaptic plasticity; cholinergic lesion; 192-IgG-saporin; hippocampus;

D O I：

10.1016/S0006-8993(02)02935-9

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

Long-term potentiation (LTP) in the hippocampal CA1 region is widely regarded to be the cellular substrate of learning and memory, and its induction critically depends on the activation of N-methyl-D-aspartate receptors (NMDARs). Nicotine reverses memory deficits caused by a lesion of the cholinergic system in animals. The mechanisms underlying this effect and the effect of nicotine on LTP after cholinergic degeneration are unknown. Here we show that cholinergic lesions impaired the induction of LTP, and nicotine reversed this effect and promoted the induction of LTP. The compensatory action of nicotine appears to be due to the enhancement of NMDAR responses mediated by nicotine-induced disinhibition of pyramidal cells. This may represent the cellular basis of nicotine-mediated cognitive enhancement observed in the presence of cholinergic deficits. (C) 2002 Elsevier Science B.V. All rights reserved.

引用

页码：148 / 152

页数：5

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