Journal Title
Title of Journal: Neurochem Res
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Abbravation: Neurochemical Research
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Authors: Hongen Wei Yuehong Ma Caiyun Ding Guorong Jin Jianrong Liu Qiaoqiao Chang Fengyun Hu Li Yu
Publish Date: 2016/08/19
Volume: 41, Issue: 11, Pages: 3129-3137
Abstract
Autism spectrum disorder ASD is a developmental disorder characterized by impairments in social and communication abilities as well as by restricted and repetitive behaviors The BTBR T + Itpr3 tf BTBR mice have emerged as a well characterized and widely used mouse model of a range of ASDlike phenotype showing deficiencies in social behaviors and unusual ultrasonic vocalizations as well as increased repetitive selfgrooming However the inherited neurobiological changes that lead to ASDlike behaviors in these mice are incompletely known and still under active investigation The aim of this study was to further evaluate the structure and neurotransmitter release of the glutamatergic synapse in BTBR mice C57BL/6J B6 mice were used as a control strain because of their high level of sociability The important results showed that the evoked glutamate release in the cerebral cortex of BTBR mice was significantly lower than in B6 mice And the level of vesicle dockingrelated protein Syntaxin1A was reduced in BTBR mice However no significant changes were observed in the number of glutamatergic synapse level of synaptic proteins density of dendritic spine and postsynaptic density between BTBR mice and B6 mice Overall our results suggest that abnormal vesicular glutamate activity may underlie the ASD relevant pathology in the BTBR miceThis work was supported by grants from National Natural Science Foundation of China No 81201061 the Ministry of Human Resources and Social Security of China No 2014 Shanxi Scholarship Council of China No 2013124 Natural Science Foundation of Shanxi No 20130210362 and Outstanding Youth Talents Program of Shanxi Province
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