2016年1月
Voltage-gated calcium and sodium channels mediate Sema3A retrograde signaling that regulates dendritic development
BRAIN RESEARCH
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- 巻
- 1631
- 号
- 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.
- リンク情報
- ID情報
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- DOI : 10.1016/j.brainres.2015.11.034
- ISSN : 0006-8993
- eISSN : 1872-6240
- PubMed ID : 26638837
- Web of Science ID : WOS:000370096700012