Glucocorticoids and lithium reciprocally regulate the proliferation of adult dentate gyrus-derived neural precursor cells through GSK-3beta and beta-catenin/TCF pathway

Boku, Shuken; Nakagawa, Shin; Masuda, Takahiro; Nishikawa, Hiroyuki; Kato, Akiko; Kitaichi, Yuji; Inoue, Takeshi; Koyama, Tsukasa

Glucocorticoids and lithium reciprocally regulate the proliferation of adult dentate gyrus-derived neural precursor cells through GSK-3beta and beta-catenin/TCF pathway

Boku, Shuken; Nakagawa, Shin; Masuda, Takahiro et al.

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2009, 34(3), 805-815

Permalink : https://hdl.handle.net/2115/50392

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アクセス権	open access
URI	https://hdl.handle.net/2115/50392
タイトル	Glucocorticoids and lithium reciprocally regulate the proliferation of adult dentate gyrus-derived neural precursor cells through GSK-3beta and beta-catenin/TCF pathway
著者	Boku, Shuken ; Nakagawa, Shin ; Masuda, Takahiro ; Nishikawa, Hiroyuki ; Kato, Akiko ; Kitaichi, Yuji ; Inoue, Takeshi ; Koyama, Tsukasa
e-Rad_Researcher 60455665 著者名 Boku, Shuken
e-Rad_Researcher 60360905 著者名 Nakagawa, Shin
著者名 Masuda, Takahiro
著者名 Nishikawa, Hiroyuki
著者名 Kato, Akiko
著者名 Kitaichi, Yuji
e-Rad_Researcher 70250438 著者名 Inoue, Takeshi
e-Rad_Researcher 10113557 著者名 Koyama, Tsukasa
言語	英語
キーワード	Neurogenesis
	Stress
	Hippocampus
	Dexamethasone
	Mood stabilizer
	Wnt
発行日	2009-02
収録物名	Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
巻(号)	34(3)
ページ	805-815
抄録	Adult hippocampal neurogenesis is decreased in rodent models for stress-related disorders at least partly through an elevated level of glucocorticoids. On the other hand, the mood stabilizer lithium (Li) commonly used for their treatment increases it. This effect is thought to be one of the therapeutic actions of Li, but the molecular mechanism has been poorly understood. Here we established the culture system of adult rat dentate gyrus-derived neural precursor cells (ADPs) and examined the effects of dexamethasone (DEX), an agonist of glucocorticoids receptor, and Li on ADP proliferation. It is possible for ADP to be a type 2a cell, which corresponds to the second stage in a model of four differentiation stages in adult hippocampal neural precursor cells. DEX decreased ADP proliferation, but Li did not have any effect on it. However, Li recovered ADP proliferation decreased by DEX. The recovery effect of Li was abolished by quercetin, an inhibitor of beta-catenin/TCF pathway. The intranuclear translocation of beta-catenin and expression of cyclin D1 are reciprocally regulated by DEX and Li in a way similar to proliferation. In addition, DEX increased the phosphorylation of Tyr(216), which renders glycogen synthase kinase-3beta (GSK-3beta) active on it. These results suggest that GSK-3beta and beta-catenin/TCF pathway might be important in the reciprocal effects between DEX and Li on ADP proliferation and are new targets of therapeutic agents for stress-related disorders.
資源タイプ	学術雑誌論文
出版タイプ	Accepted Manuscript
PISSN	1740-634X
関連情報	PMID 19005466
関連情報 (isVersionOf)	出版社版DOI https://doi.org/10.1038/npp.2008.198