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Titolo:
Nicotine accelerates reversal of long-term potentiation and enhances long-term depression in the rat hippocampal CA1 region
Autore:
Fujii, S; Sumikawa, K;
Indirizzi:
Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA Univ CalifIrvine Irvine CA USA 92697 obiol & Behav, Irvine, CA 92697 USA Yamagata Univ, Sch Med, Dept Physiol, Yamagata 99023, Japan Yamagata UnivYamagata Japan 99023 , Dept Physiol, Yamagata 99023, Japan
Titolo Testata:
BRAIN RESEARCH
fascicolo: 2, volume: 894, anno: 2001,
pagine: 340 - 346
SICI:
0006-8993(20010316)894:2<340:NAROLP>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
RABBIT FOLLOWING STIMULATION; ACETYLCHOLINE-RECEPTORS; SYNAPTIC TRANSMISSION; LASTING POTENTIATION; COGNITIVE FUNCTION; PERFORANT PATH; ACH RECEPTORS; DENTATE GYRUS; KINASE-II; INTERNEURONS;
Keywords:
nicotinic acetylcholine receptor; nicotine; methyllycaconitine; long-term potentiation; depotentiation; long-term depression; synaptic plasticity; hippocampus;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Sumikawa, K Univ Calif Irvine, Dept Neurobiol & Behav, Irvine, CA 92697 USA Univ Calif Irvine Irvine CA USA 92697 v, Irvine, CA 92697 USA
Citazione:
S. Fujii e K. Sumikawa, "Nicotine accelerates reversal of long-term potentiation and enhances long-term depression in the rat hippocampal CA1 region", BRAIN RES, 894(2), 2001, pp. 340-346

Abstract

In the hippocampal CA1 region, low-frequency stimulation (LFS; 200 pulses at 1 Hz) causes reversal of long-term potentiation (depotentiation, DP) andlong-term depression (LTD), both of which are thought to be the cellular substrate of learning and memory. Because nicotine enhances learning and memory, we examined if nicotine modulates DP and LTD in the hippocampal CA1 region. Bath application of nicotine during LFS accelerated DP, that is, potentiated synaptic responses in hippocampal CA1 neurons returned to pre-tetanic control levels more rapidly in the presence of nicotine. Because a similar acceleration of DP was observed using the alpha7 nicotinic acetylcholinereceptor (nAChR)-selective antagonist methyllcaconitine (MLA), the nicotine effect appeared to be at least partly mediated by nicotine-induced desensitization of alpha7 nAChRs. Delivery of LFS in the presence of nicotine or MLA also depressed synaptic responses in a naive pathway and facilitated LTD, that is, the magnitude of LTD was larger when the drug was present during LFS. Thus, these results demonstrate that nicotine facilitates DP and LTD, which may represent, at least in part, the cellular mechanism underlying nicotine-induced cognitive enhancement. (C) 2001 Elsevier Science B.V. All rights reserved.

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Documento generato il 10/04/20 alle ore 16:09:59