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Shaohua Xu, 1–3,* Yiyun Liu, 2, 3,* Juncai Pu, 2, 3,* Siwen Gui, 2–4,* Xiaogang Zhong, 2, 3 Lu Tian, 2, 3 Xuemian Song, 2–4 Xunzhong Qi, 2, 3 Haiyang Wang, 2, 3 Peng Xie 1–3, 5 1Department of Neurology, Yongchuan Hospital, Chongqing Medical University, Chongqing 402160, People’s Republic of China; 2NHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People’s Republic of China; 3Chongqing Key Laboratory of Neurobiology, Chongqing 400016, People’s Republic of China; 4College of Biomedical Engineering, Chongqing Medical University, Chongqing 400016, People’s Republic of China; 5Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, People’s Republic of China*These authors contributed equally to this workCorrespondence: Peng XieNHC Key Laboratory of Diagnosis and Treatment on Brain Functional Diseases, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, People’s Republic of ChinaTel +86-023-68485490Fax +86-023-68485111Email xiepeng@cqmu.edu.cnBackground: Major depressive disorder (MDD) is a complex psychiatric illness involving multiple brain regions. Increasing evidence indicates that the striatum is involved in depression, but the molecular mechanisms remain unclear.Methods: In this study, we performed a gas chromatography–mass spectrometer (GC/MS)-based metabolomic analysis in the striatum of depressed rats induced by chronic unpredictable mild stress (CUMS). We then compared striatal data with our previous data from the hippocampus and cerebellum to systematically investigate the potential pathogenesis of depression.Results: We identified 22 differential metabolites in the striatum between the CUMS and control groups; these altered metabolites were mainly involved in amino acid, carb

Chenmeng Li,1–3,* Xiaoyan Xu,2–4,* Xiong Zhang,2–4,* Ke Cheng,2,3,* Yujie Guo,1–3 Jie Jie,1–3 Hua Guo,1–3 Yong He,1–3 Chanjuan Zhou,2,3 Siwen Gui,2,3 Xiaogang Zhong,2,3 Haiyang Wang,2–4 Peng Xie1–4 1Department of Neurology, Yongchuan Hospital of Chongqing Medical University, Chongqing 402460, China; 2Department of Neurology Institute of Neuroscience and Collaborative Innovation Center for Brain Science, Chongqing Medical University, Chongqing 400016, China; 3Chongqing Key Laboratory of Neurobiology, Chongqing 400016, China; 4Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China *These authors contributed equally to this work Background: Neuropsychiatric disorders are devastating illnesses worldwide; however, the potential involvement of viruses in the pathophysiological mechanisms of psychiatric diseases have not been clearly elucidated. Borna disease virus (BDV) is a neurotropic, noncytopathic RNA virus. Materials and methods: In this study, we infected neonatal rats intracranially with BDV Hu-H1 and Strain V within 24 hours of birth. Psychological phenotypes were assessed using sucrose preference test, open field test, elevated plus maze test, and forced swim test. The protein expression of ERK/CREB/BDNF pathway was assessed by Western blotting of in vitro and in vivo samples. Results: Hu-H1-infected rats showed anxiety-like behavior 8 weeks postinfection while Strain V-infected rats demonstrated a certain abnormal behavior. Phosphorylated ERK1/2 was significantly upregulated in the hippocampi of Strain V- and Hu-H1-infected rats compared with control rats, indicating that Raf/MEK/ERK signaling was activated. Conclusion: The data suggested that infection of neonatal rats with BDV Hu-H1 and Strain V caused behavioral abnormalities that shared common molecular pathways, providing preliminary evidences to investi