Abstract #0640
Astrocyte dysfunction drives abnormal resting-state functional connectivity in depression
Jiaming Liu1, Jia-Wen Mo2, Xunda Wang3,4, Ziqi An1, Shuangyang Zhang1, Can-Yuan Zhang2, Peiwei Yi1, Alex T. L. Leong3,4, Jing Ren2, Liang-Yu Chen2, Ran Mo2, Yuanyao Xie1, Qianjin Feng1, Wufan Chen1, Tian-Ming Gao2, Ed X. Wu3,4, Yanqiu Feng1,2,5,6, and Xiong Cao2,7
1School of Biomedical Engineering, Southern Medical University, Guangzhou, China, Guangzhou, China, 2Key Laboratory of Mental Health of the Ministry of Education, Guangdong-Hong Kong-Macao Greater Bay Area Center for Brain Science and Brain-Inspired Intelligence, Guangdong Province Key Laboratory of Psychiatric Disorders, Department of Neurobiology, School of Basic Medical Sciences, Southern Medical University, Guangzhou 510515, China, Guangzhou, China, 3Laboratory of Biomedical Imaging and Signal Processing, The University of Hong Kong, Pokfulam, Hong Kong SAR, China, Hong Kong, China, 4Department of Electrical and Electronic Engineering, The University of Hong Kong, Pokfulam, Hong Kong SAR, China, Hong Kong, China, 5Guangdong Provincial Key Laboratory of Medical Image Processing, Southern Medical University, Guangzhou, China, Guangzhou, China, 6Guangdong Province Engineering Laboratory for Medical Imaging and Diagnostic Technology, Southern Medical University, Guangzhou, China, Guangzhou, China, 7Microbiome Medicine Center, Department of Laboratory Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China, Guangzhou, China
Synopsis
Keywords: Brain Connectivity, fMRIEven though brain-wide network-level abnormalities in major depressive disorder (MDD) patients via resting-state functional MRI (rsfMRI) exist, the mechanisms underlying such network changes are unknown. Here, we show that the astrocytic calcium deficient mice, inositol 1,4,5-trisphosphate-type-2 receptor knockout mice (Itpr2-/- mice), display abnormal rsfMRI connectivity (rsFC), which is highly consistent with those of MDD patients. Optogenetic activation of medial prefrontal cortex (mPFC) astrocytes partially rescues rsFC. Optogenetic activation of the mPFC neurons or mPFC-striatum pathway rescues disrupted rsFC and depressive-like behaviors in Itpr2-/- mice. Our results identify the previously unknown role of astrocyte dysfunction in driving rsFC abnormalities in depression.
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