Chronic electroconvulsive seizure up-regulates β-catenin expression in rat hippocampus:: Role in adult neurogenesis

被引:110
作者
Madsen, TM
Newton, SS
Eaton, ME
Russell, DS
Duman, RS
机构
[1] Yale Univ, Sch Med, Connecticut Mental Hlth Ctr, Lab Mol Psychiat,Dept Psychiat, New Haven, CT 06508 USA
[2] Yale Univ, Sch Med, Dept Pharmacol, New Haven, CT 06508 USA
关键词
antidepressant; Wnt signaling; immunohistochemistry; seizure; GLYCOGEN-SYNTHASE KINASE-3-BETA; TRANSGENIC MICE; WNT; GSK-3-BETA; SIGNAL; BRAIN; DIFFERENTIATION; THERAPY; NEURONS; CELLS;
D O I
10.1016/S0006-3223(03)00700-5
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Background: Beta-catenin was discovered as a cytoskeletal protein, constituting a link between the cadherins to the actin cytoskeleton. Aside from this function, beta-catenin is a key effector molecule in the Wnt signaling pathway, serving as a downstream transcription factor. Methods: In this study, we examined the influence of electroconvulsive seizures (ECS) on the expression of beta-catenin, as well as expression of Wnt-2, in rat hippocampus. Repeated administration of generalized seizures increased levels of beta-catenin immunoreactivity in the subgranular zone of the hippocampus. To assess the relationship of beta-catenin to cell division in the dentate gyrus of the adult rat hippocampus, colocalization of beta-catenin with a marker of cell division was examined. Results: Beta-catenin immunoreactivity was consistently localized in newborn cells in this region, indicating a possible role in cell division and differentiation in adult hippocampus. We also found that ECS treatment significantly increased levels of Wnt-2, one of the ligands that activates beta-catenin signaling. Conclusions: These results demonstrate that ECS increases Wnt-beta-catenin signaling and suggest that this pathway could mediate in part the neuronal adaptations underlying the therapeutic action of this treatment paradigm. Biol Psychiatry 2003;54:1006-1014 (C) 2003 Society of Biological Psychiatry
引用
收藏
页码:1006 / 1014
页数:9
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