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Reversing neural circuit and behavior deficit in mice exposed to maternal inflammation by Zika␣virus.

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机构： [1]Center for Craniofacial Molecular Biology, University of Southern California (USC), Los Angeles, CA, USA. [2]Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, USA. [3]Department of Anesthesiology and Pain Medicine, the University of Texas MD Anderson Cancer Center, Houston, TX, USA. [4]State Key Laboratory of Oral Diseases, National Clinical Research Center for Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, China. [5]College of Stomatology, Chongqing Medical University, Chongqing, China. [6]Department of Human Genetics, Emory University School of Medicine, Atlanta, GA, USA. [7]Department of Diagnostic Radiology and Nuclear Medicine, University of Maryland School of Medicine, Baltimore, MD, USA. [8]Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. [9]Department of Pathology and Anatomy, Eastern Virginia Medical School, Norfolk, VA, USA. [10]Department of Microbiology and Molecular Cell Biology, Eastern Virginia Medical School, Norfolk, VA, USA.

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关键词： chemogenetics mouse behaviors neural circuit Zika virus

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Zika virus (ZIKV) infection during pregnancy is linked to various developmental brain disorders. Infants who are asymptomatic at birth might have postnatal neurocognitive complications. However, animal models recapitulating these neurocognitive phenotypes are lacking, and the circuit mechanism underlying behavioral abnormalities is unknown. Here, we show that ZIKV infection during mouse pregnancy induces maternal immune activation (MIA) and leads to autistic-like behaviors including repetitive self-grooming and impaired social memory in offspring. In the medial prefrontal cortex (mPFC), ZIKV-affected offspring mice exhibit excitation and inhibition imbalance and increased cortical activity. This could be explained by dysregulation of inhibitory neurons and synapses, and elevated neural activity input from mPFC-projecting ventral hippocampus (vHIP) neurons. We find structure alterations in the synaptic connections and pattern of vHIP innervation of mPFC neurons, leading to hyperconnectivity of the vHIP-mPFC pathway. Decreasing the activity of mPFC-projecting vHIP neurons with a chemogenetic strategy rescues social memory deficits in ZIKV offspring mice. Our studies reveal a hyperconnectivity of vHIP to mPFC projection driving social memory deficits in mice exposed to maternal inflammation by ZIKV.© 2021 The Authors.

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出版当年[2021]版：

大类 | 1 区

生物学

小类 | 2 区生化与分子生物学 2 区细胞生物学

最新[2023]版：

大类 | 1 区

生物学

小类 | 2 区生化与分子生物学 2 区细胞生物学

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第一作者机构： [1]Center for Craniofacial Molecular Biology, University of Southern California (USC), Los Angeles, CA, USA.

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