in vivo and in vitro have demonstrated the relationship of depression with neuroinflammation mediated by microglial polarization. The possible mechanisms of polarization mediating depression involve NF-κB signaling pathway activation, respiratory bursts, complement receptor 3 (CR3) signaling pathway activation, NLRP3 inflammation activation, cannibalism receptor 1 (CB1) activation, Notch-1 signal pathway stimulation, and PPARγ receptor activation. This review discusses research progress on the relationship between microglial polarization and depression.]]> 2021/12/23 13:40:43 WAN Teng,GAO Xue,LIU Shun-Feng,MENG An-Na,Lü Hong-Ying,WU Zhuan and ZHOU Shou-Hong 5true Crtc1 knockout (Crtc1^-/-) mice were first successfully prepared in 2012 and Crtc1^-/- mice exhibited a depression-like behavioral phenotype, the growing clues suggest that CRTC1 is involved in depression. Our previous work demonstrates that knockdown of CRTC1 in hippocampal dentate gyrus directly induced depression-like behavior in mice. Downregulation of CRTC1 expression in hippocampus is associated with depression-like behaviors in CUMS (chronic unpredictabk mild stress), CSDS (chronic social defeat stress) and CRS (chronic restrain stress) mouse models, LPS(lipopolysaccharide)-treated mouse model and prenatal stress-induced depression model in offspring rats. Furthermore, abnormal CRTC1 expression or activation may be involved in depression-like behavior via SIK2/CRTC1/CREB/BDNF pathway, CRTC1/BDNF/TrkB/VGF pathway, agmatinergic system and neuroinflammation. In addition, Crtc1^-/- mice are shown to be resistant to the antidepressant effects of the tricyclic antidepressants such as fluoxetine, desipramine, venlafaxine and imipramine etc., suggesting that CRTC1 alterations may be related with treatment-resistant depression. Histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) partially rescues the depression-like behavior of Crtc1^-/- mice accompanied by an increased expression of BDNF, the effects are mediated by CRTC1. Although CRTC1 expression is disturbed in the brain of depression-related models, whether and how it is involved in the process of neurogenesis and neuroplasticity impairments in depression still needs further research. This article reviews the research of CRTC1 in depression from the aspects of behavior, related signal pathways and participation in the role of antidepressants.]]> 2021/12/23 13:40:43 LI De-Zhu,NI Sai-Qi,ZHANG Min-Jian,LU Si-Yi,LIU Xin-Lan and ZHANG Jun-Fang 4true 2021/12/23 13:40:45 CHEN Hong-Li,GAO Jing-Jing,YANG Jia-Jia,JIANG Zhong-Di,CHEN Rui-Juan,LIU Shuang and MING Dong 3true via intrinsically photosensitive retinal ganglion cells to perihabenular nucleus (ipRGC-PHb) pathway. A recent report demonstrated that activation of the disynaptic retina-vLGN/IGL-LHb pathway underlies the anti-depressive effects of light therapy. Monoamine neurotransmitter as well as cortisol are also involved in regulating depressive-like behaviors during light therapy. The current review provides potentially theoretical basis for the optimization and promotion of light therapy in anti-depression.]]> 2021/12/23 13:40:46 CUI Ke-Ke,JIN Lei,JIN Bin-Jie,WANG Zhi-Kai,WANG Xiang-Qun,ZOU Dan-Dan and WANG Zheng-Chun 2true 2+ activity and ATP release. Our previous work has demonstrated that Calhm2 plays a crucial role in the progression of depression by regulating the astrocytic ATP release. In order to further explore the role and mechanism of Calhm2 in the development of depression, we firstly predicted the ATP binding site (glutamine, amino acid 87) of Calhm2, and established a mouse line that carried calhm2 mutation by mutating the glutamine to alanine (Q87A). Secondly, by using the primary culture of astrocyte and ATP detection analysis, we found that Calhm2 Q87A mutation resulted in a significant decrease of ATP release in astrocytes. Furthermore, we found that the ATP release decreased in hippocampal slice from Calhm2 Q87A mutated mice. Importantly, Calhm2 Q87A mutated mice showed a higher susceptibility to develop depression-like symptoms than that of wild type mice when exposed to chronic unpredictable mild stress (CUMS). Taken together, we identified that Q87 site is important for Calhm2-mediated ATP release in astrocytes and this point mutation of Calhm2 promotes depression susceptibility induced by stress in mice. The present work further defines the molecular mechanism of Calhm2 in the development of depression, with the implication of a potential avenues for the diagnosis and therapeutics of depression-related diseases.]]> 2021/12/23 13:40:49 LIAO Yang,PAN Rui-Yuan and YUAN Zeng-Qiang 1true