Involvement of endogenous PACAP expression in the activity-dependent survival of mouse cerebellar granule cells

Akiko Tabuchi, Motoko Koizumi, Jun Nakatsubo, Takahiro Yaguchi, Masaaki Tsuda*

*この論文の責任著者

研究成果: ジャーナルへの寄稿学術論文査読

40 被引用数 (Scopus)

抄録

Membrane depolarization causes Ca2+ influx through L-type voltage-dependent calcium channels (L-VDCC), which promotes the activity-dependent survival of mouse cerebellar granule cells (CGCs). Although exogenously added pituitary adenylate cyclase activating polypeptide (PACAP) is effective in promoting the survival of CGCs, it is unknown whether PACAP is synthesized in CGCs and involved in the activity-dependent survival of CGCs. In this study, we found that the PACAP gene was activated in depolarized CGCs cultured at 25 mM KCl (high K+), independently of de novo protein synthesis. In addition, the PACAP immunoreactivity increased through the activation of L-VDCC in depolarized CGCs, indicating that PACAP is concomitantly produced with PACAP mRNA in an activity-dependent manner. Exogenously added PACAP attenuated the apoptosis of CGCs through a specific interaction with PACAP receptors. Furthermore, a PACAP receptor antagonist, PACAP(6-38), reduced the survival of CGCs at high K+. These findings indicate that endogenous PACAP production induced by Ca2+ signals exerts a survival effect on CGCs via PACAP receptors, which, at least in part, accounts for the activity-dependent survival of CGCs.

本文言語英語
ページ(範囲)85-93
ページ数9
ジャーナルNeuroscience Research
39
1
DOI
出版ステータス出版済み - 2001

ASJC Scopus 主題領域

  • 神経科学一般

フィンガープリント

「Involvement of endogenous PACAP expression in the activity-dependent survival of mouse cerebellar granule cells」の研究トピックを掘り下げます。これらがまとまってユニークなフィンガープリントを構成します。

引用スタイル