論文

査読有り
2015年9月

INFLUX OF EXTRACELLULAR ZN(2+) INTO THE HIPPOCAMPAL CA1 NEURONS IS REQUIRED FOR COGNITIVE PERFORMANCE VIA LONG-TERM POTENTIATION

NEUROSCIENCE
  • A. Takeda
  • ,
  • M. Suzuki
  • ,
  • M. Tempaku
  • ,
  • K. Ohashi
  • ,
  • H. Tamano

304
開始ページ
209
終了ページ
216
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.neuroscience.2015.07.042
出版者・発行元
PERGAMON-ELSEVIER SCIENCE LTD

Physiological significance of synaptic Zn2+ signaling was examined in the CA1 of young rats. In vivo CA1 long-term potentiation (LTP) was induced using a recording electrode attached to a microdialysis probe and the recording region was locally perfused with artificial cerebrospinal fluid (ACSF) via the microdialysis probe. In vivo CA1 LTP was inhibited under perfusion with CaEDTA and ZnAF-2DA, extracellular and intracellular Zn2+ chelators, respectively, suggesting that the influx of extracellular Zn2+ is required for in vivo CA1 LTP induction. The increase in intracellular Zn2+ was chelated with intracellular ZnAF-2 in the CA1 1 h after local injection of ZnAF-2DA into the CA1, suggesting that intracellular Zn2+ signaling induced during learning is blocked with intracellular ZnAF-2 when the learning was performed 1 h after ZnAF-2DA injection. Object recognition was affected when training of object recognition test was performed 1 h after ZnAF-2DA injection. These data suggest that intracellular Zn2+ signaling in the CA1 is required for object recognition memory via LTP. Surprisingly, in vivo CA1 LTP was affected under perfusion with 0.1-1 mu M ZnCl2, unlike the previous data that in vitro CA1 LTP was enhanced in the presence of 1-5 mu M ZnCl2. The influx of extracellular Zn2+ into CA1 pyramidal cells has bidirectional action in CA1 LTP. The present study indicates that the degree of extracellular Zn2+ influx into CA1 neurons is critical for LTP and cognitive performance. (C) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.

Web of Science ® 被引用回数 : 20

リンク情報
DOI
https://doi.org/10.1016/j.neuroscience.2015.07.042
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26204819
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000360008800019&DestApp=WOS_CPL

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