Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis. (Molecular Psychiatry (2014) 19, 699–709)

報告日期: 2015/11/20
報告時間: 4:00/4:50
報告學生: 鍾宜倫
講評老師: 莊季瑛
附件下載: 下載[1526-1443055689-1.pdf] 

Dynamic microglial alterations underlie stress-induced depressive-like behavior and suppressed neurogenesis

Molecular Psychiatry (2014) 19, 699–709

Speaker: Chung Yi-Lun (鍾宜倫)          Location: Room 602

Commentator: Prof. Jih-Ing Chuang       Time: 2015/11/20, 16:00~16:50 


Over the past decade, it is well known in molecular, cellular and neuron function of major depression. Moreover, microglial activation and brain inflammatory cytokines have also been implicated in mediating the effects of stress, which has been implicated as a major trigger for depression. Herein, the authors examined the role of dynamic alterations in microglia activation status in the development of chronic unpredictable stress (UCS)-induced depressive-like condition.

The authors found that in short term period (2–3 days), stress induced microglial proliferation and activation, while reduction in microglial numbers was found following 5 weeks of CUS exposure in the hippocampus, but not in other brain regions. Antidepressant drug imipramine or microglial inhibitor minocycline or by transgenic interleukin-1 receptor antagonist overexpression blocked initial stress-induced microglial activation, as well as the CUS-induce microglial decline and depressive-like behavior. Treatment of CUS-exposed mice with LPS, or macrophage colony-stimulating factor (M-CSF) or granulocyte-macrophage colony-stimulating factor (GM-CSF) stimulated hippocampal microglial proliferation and reversed the depressive-like behavior and increased hippocampal neurogenesis. These results provide directly evidence that disturbances in microglial functioning plays an important role in chronic stress-induced depression, suggesting that microglia stimulators could serve as fast-acting antidepressants in some forms of stress-related depression.  


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