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

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Title: Glucocorticoids and lithium reciprocally regulate the proliferation of adult dentate gyrus-derived neural precursor cells through GSK-3beta and beta-catenin/TCF pathway
Authors: Boku, Shuken Browse this author →KAKEN DB
Nakagawa, Shin Browse this author →KAKEN DB
Masuda, Takahiro Browse this author
Nishikawa, Hiroyuki Browse this author
Kato, Akiko Browse this author
Kitaichi, Yuji Browse this author
Inoue, Takeshi Browse this author →KAKEN DB
Koyama, Tsukasa Browse this author →KAKEN DB
Keywords: Neurogenesis
Stress
Hippocampus
Dexamethasone
Mood stabilizer
Wnt
Issue Date: Feb-2009
Journal Title: Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
Volume: 34
Issue: 3
Start Page: 805
End Page: 815
Publisher DOI: 10.1038/npp.2008.198
PMID: 19005466
Abstract: 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.
Type: article (author version)
URI: http://hdl.handle.net/2115/50392
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 朴 秀賢

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