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Astrocytic Kir4.1 regulates NMDAR/calpain signaling axis in l
Custom-Made AAVs were used for gene knockdown. (From BrainVTA)
The viruses used in this article from BrainVTA are in the table below
Custom-Made AAV  PT-2054-AAV2/5 GFAP-EGFP-shRNA Kir4.1
 AAV2/5-GFAP-EGFP-shRNA scramble
Zhujin Song, Zhijuan Bian, Zhengrong Zhang, Xuncui Wang, Aisong Zhu, Guoqi Zhu
Pub Date: 2021-08-30, DOI: 10.1016/j.taap.2021.115711, Email: [email protected]
The activation of Nod-like receptor protein 3 (NLRP3) inflammasome propagates pro-inflammatory signaling cascades linking to depression-like behaviors. However, the signaling pathway contributing to NLRP3 inflammasome activation and depression-like behaviors is still not clear. In this study, we evidenced that lipopolysaccharide (LPS) injection (i.p.) triggered depression-like behaviors, promoted the expression of Kir4.1, p-GluN2B and calpain-1, and activated NLRP3 inflammasome. The blockage of N-methyl-d-aspartate receptors (NMDAR) by memantine reduced LPS-induced depression-like behaviors, NLRP3 inflammasome and astrocyte activation, and calpain-1 expression. Additionally, memantine also inhibited LPS-induced reduction of postsynaptic density protein 95 (PSD-95) and Arc expression. Specific reduction of Kir4.1 in astrocytes attenuated LPS-induced expression of NLRP3 and calpain-1, and phosphorylation of GluN2B. Interestingly, LPS-induced expression of calpain-1 largely co-localized with GFAP, indicating the specific function of calpain-1 in astrocytes. Together, these data indicate that astrocytic Kir4.1 could regulate NMDAR/calpain-1 signaling axis, contributing to depression-like behaviors, likely through regulating NLRP3 inflammasome activation.
In this study, the authors used LPS-induced depression model to evaluate the astrocytic Kir4.1 and NMDAR/calpain-1 signaling axis in the pathogenesis of depression, so as to provide important molecular targets for diagnosis and treatment of depression.
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