論文

査読有り
2016年1月

Voltage-gated calcium and sodium channels mediate Sema3A retrograde signaling that regulates dendritic development

BRAIN RESEARCH
  • Naoya Yamashita
  • ,
  • Reina Aoki
  • ,
  • Sandy Chen
  • ,
  • Aoi Jitsuki-Takahashi
  • ,
  • Shunsuke Ohura
  • ,
  • Haruyuki Kamiya
  • ,
  • Yoshio Goshima

1631
開始ページ
127
終了ページ
136
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.brainres.2015.11.034
出版者・発行元
ELSEVIER SCIENCE BV

Growing axons rely on local signaling at the growth cone for guidance cues. Semaphorin3A (Sema3A), a secreted repulsive axon guidance molecule, regulates synapse maturation and dendritic branching. We previously showed that local Sema3A signaling in the growth cones elicits retrograde retrograde signaling via PlexinA4 (PlexA4), one component of the Sema3A receptor, thereby regulating dendritic localization of AMPA receptor G1uA2 and proper dendritic development. In present study, we found that nimodipine (voltage-gated L-type Ca2+ channel blocker) and tetrodotoxin (TTX; voltage-gated Na+ channel blocker) suppress Sema3A-induced dendritic localization of GluA2 and dendritic branch formation in cultured hippocampal neurons. The local application of nimodipine or TTX to distal axons suppresses retrograde transport of Venus-Sema3A that has been exogenously applied to the distal axons. Sema3A facilitates axonal transport of PlexA4, which is also suppressed in neurons treated with either TTX or nimodipine. These data suggest that voltage-gated calcium and sodium channels mediate Sema3A retrograde signaling that regulates dendritic GluA2 localization and branch formation. (C) 2015 Elsevier B.V. All rights reserved.

Web of Science ® 被引用回数 : 5

リンク情報
DOI
https://doi.org/10.1016/j.brainres.2015.11.034
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/26638837
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000370096700012&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.brainres.2015.11.034
  • ISSN : 0006-8993
  • eISSN : 1872-6240
  • PubMed ID : 26638837
  • Web of Science ID : WOS:000370096700012

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