Key Laboratory of the Health Ministry for Forensic Medicine

Fengcheng, China

Key Laboratory of the Health Ministry for Forensic Medicine

Fengcheng, China
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Li B.-J.,Xi'an Jiaotong University | Liu P.,Xi'an Jiaotong University | Chu Z.,Xi'an Jiaotong University | Shang Y.,Xi'an Jiaotong University | And 4 more authors.
NeuroReport | Year: 2017

Both genetic factors and early life adversity play major roles in the etiology of schizophrenia. Our previous studies indicated that social isolation (SI) during early postnatal development leads to several lasting abnormal behavioral and pathophysiological features resembling the core symptoms of some human neuropsychiatric disorders in mice. The glutamate and dopamine hypotheses are tightly linked to the development of schizophrenia. The cross-talk between glutamate N-methyl-d-aspartate acid receptors and dopamine receptors is associated with histidine triad nucleotide binding protein 1 (HINT1), which is correlated with diverse psychiatric disorders. We examined the effects of SI on schizophrenia-like behavior and used enzyme-linked immunosorbent assays to investigate the expression levels of HINT1, the NR1 subunit of N-methyl-d-aspartate acid receptor, and dopamine type 2 receptor (D2R) in C57 mice. We found that SI leads to a series of schizophrenia-related deficits, such as social withdrawal, anxiety disorder, cognitive impairments, and sensorimotor gating disturbances. These abnormal phenotypes paralleled changes of HINT1, NR1, and D2R. SI may be considered a robust model of the effects of early life stress on the schizophrenia-related behaviors in mice. Potential interactions among HINT1, NR1, and D2R may underlie the behavioral deficits induced by SI. Copyright © 2017 The Author(s). Published by Wolters Kluwer Health, Inc.


Chen Y.-J.,Xi'an Jiaotong University | Liu Y.-L.,Key Laboratory of the Health Ministry for Forensic Medicine | Zhong Q.,Key Laboratory of the Health Ministry for Forensic Medicine | Yu Y.-F.,University of Georgia | And 6 more authors.
Neuroscience Bulletin | Year: 2012

Objective: The purpose of this study was to investigate the effect of methamphetamine (MA) on spatial learning and memory and the role of tetrahydropalmatine (THP) in MA-induced changes in these phenomena in mice. Methods: Male C57BL/6 mice were randomly divided into eight groups, according to different doses of MA, different doses of THP, treatment with both MA and THP, and saline controls. Spatial learning and memory were assessed using the Morris water maze. Western blot was used to detect the expression of extracellular signal-regulated protein kinase (ERK) in the mouse prefrontal cortex (PFC) and hippocampus. Results: Repeated MA treatment significantly increased the escape latency in the learning phase and decreased the number of platform site crossings in the memory-test phase. ERK1/2 expression was decreased in the PFC but not in the hippocampus of the MA-treated mice. Repeated THP treatment alone did not affect the escape latency, the number of platform site crossings or the total ERK1/2 expression in the brain. Statistically significantly shorter escape latencies and more platform site crossings occurred in MA+THP-treated mice than in MA-treated mice. Conclusion: Repeated MA administration impairs spatial learning and memory in mice, and its co-administration with THP prevents this impairment, which is probably attributable to changed ERK1/2 expression in the PFC. This study contributes to uncovering the mechanism underlying MA abuse, and to exploring potential therapies. © Shanghai Institutes for Biological Sciences, CAS and Springer-Verlag Berlin Heidelberg 2012.

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