Inactivation of α7 ACh receptors and activation of non-α7 ACh receptors both contribute to long term potentiation induction in the hippocampal CA1 region

被引:90
|
作者
Fujii, S
Ji, ZX
Sumikawa, K [1 ]
机构
[1] Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA
[2] Yamagata Univ, Sch Med, Dept Physiol, Yamagata 9909585, Japan
关键词
nicotinic acetylcholine receptor; nicotine; metyllycaconitine; dihydro-beta-erythroidine; A85380; long-term potentiation; hippocampus;
D O I
10.1016/S0304-3940(00)01076-4
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Acute and chronic nicotine exposure differentially facilitate the induction of long-term potentiation (LTP), a synaptic model of learning and memory, in the hippocampal CA1 region. The mechanisms underlying these effects of nicotine, however, are unknown. In the present study, both nicotinic acetylcholine receptor (nAChR) agonists and an alpha 7 nAChR antagonist facilitated the induction LTP in the hippocampal CA1 region of naive rat. Furthermore, chronic nicotine treatment lowered the threshold for induction of LTP, and acute application of nicotinic agonists, but not an alpha 7 antagonist, further facilitated LTP induction in the chronic-nicotine-treated hippocampus. These results suggest not only that both activation of non-alpha 7 nAChRs and inactivation of alpha 7 nAChRs contribute to LTP induction, but also that chronic-nicotine-mediated facilitation of LTP induction is due to chronic-nicotine-induced desensitization of alpha 7 nAChRs, (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:134 / 138
页数:5
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