Rapid spinogenesis of pyramidal neurons induced by activation of glucocorticoid receptors in adult male rat hippocampus

被引:68
作者
Komatsuzaki, Y
Murakami, G
Tsurugizawa, T
Mukai, H
Tanabe, N
Mitsuhashi, K
Kawata, M
Kimoto, T
Ooishi, Y
Kawato, S
机构
[1] Univ Tokyo, Dept Biophys & Life Sci b, Grad Sch Arts & Sci, Tokyo 153, Japan
[2] Meiji Univ, Sch Sci & Technol, Kawasaki, Kanagawa 214, Japan
[3] Univ Tokyo, Core Res Evolut Sci & Technol Project, Japan Sci & Technol Agcy, Grad Sch Arts & Sci, Tokyo 153, Japan
[4] Kyoto Prefectural Univ Med, Dept Anat & Neurobiol, Kamigyo Ku, Kyoto 6028566, Japan
关键词
stress; corticosterone; glucocorticoid; dexamethasone; spine; synapse; hippocampus;
D O I
10.1016/j.bbrc.2005.07.173
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Modulation of hippocampal synaptic plasticity by glucocorticoids has been attracting much attention, due to its importance in stress responses. Dendritic spines are essential for memory storage processes. Here, we investigated the effect of dexamethasone (DEX), a specific agonist of glucocorticoid receptor (GR), on density and morphology of dendritic spines in adult male rat hippocampus by imaging of Lucifer Yellow-injected spines in slices. The application of 100 nM DEX (stressful high concentration) induced rapid modulation of the density and morphology of dendritic spines in CA1 pyramidal neurons within 1 h. The total spine density increased from 0.88 spines/mu m (control) to 1.36 spines/mu m (DEX-treated). DEX significantly increased the density of thin and mushroom type spines, however only a slight increase was observed for stubby and filopodium type spines. Because the presence of 10 mu M cycloheximide, an inhibitor of protein synthesis, did not suppress the DEX effect, these responses are probably non-genomic. Western immunoblot analysis demonstrated the localization of classical type GR in Triton-insoluble synaptosomal fractions (enriched in postsynaptic membranes) from hippocampal slices, suggesting a possible action site of DEX at spines. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码:1002 / 1007
页数:6
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