Research Papers:

Spatial memory impairment by TRPC1 depletion is ameliorated by environmental enrichment

Renzhong Xing, Yanling Zhang, Hua Xu, Xiaobin Luo, Raymond Chuen-Chung Chang, Jianjun Liu and Xifei Yang _

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Oncotarget. 2016; 7:27855-27873. https://doi.org/10.18632/oncotarget.8428

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Renzhong Xing1,2,*, Yanling Zhang1,2,*, Hua Xu1, Xiaobin Luo4,5, Raymond Chuen-Chung Chang3, Jianjun Liu2, Xifei Yang2

1College of Pharmacy, Jinan University, Guangdong, China

2Key Laboratory of Modern Toxicology of Shenzhen, Medical Key Laboratory of Guangdong Province, Medical Key Laboratory of Health Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China

3Laboratory of Neurodegenerative Diseases, Department of Anatomy, The University of Hong Kong, Pokfulam, Hong Kong SAR, China

4AND Biotech, Shenzhen, China

5Guang Zhou Kai-Tuo Biotech, Guangzhou, China

*These authors have contributed equally to this work

Correspondence to:

Xifei Yang, e-mail: [email protected]

Hua Xu, e-mail: [email protected]

Keywords: TRPC1, memory, environment enrichment, α-internexin, GMF-β

Received: October 08, 2015     Accepted: March 08, 2016     Published: March 28, 2016


Canonical transient receptor potential (TRPC) channels are widely expressed throughout the nervous system whereas their functions remain largely unclear. Here we investigated the effects of TRPC1 deletion on spatial memory ability of mice and the potential intervention by environmental enrichment (EE). Significant spatial memory impairment assessed by conditional fearing test, Y maze test and step-down test in TRPC1 knockout mice was revealed. The behavioral abnormality were attenuated by the treatment of EE. Proteomic analysis by two-dimensional fluorescence difference gel electrophoresis (2D-DIGE) coupled with a matrix-assisted laser desorption/ionisation-time of flight (MALDI-TOF) and tandem mass spectrometry (MS) revealed that TRPC1 deletion caused differential expression of a total of 10 proteins (8 up-regulated and 2 down-regulated) in hippocampus. EE treatment resulted in differential expression of a total of 22 proteins (2 up-regulated and 20 down-regulated) in hippocampus of TRPC1 knockout mice. Among these differentially expressed proteins, the expression of α-internexin and glia maturation factor β (GMF-β), two proteins shown to impair memory, were significantly down-regulated in hippocampus of TRPC1 knockout mice by EE treatment. Taken together, these data suggested that TRPC1 regulated directly or indirectly the expression of multiple proteins, which may be crucial for the maintenance of memory ability, and that EE treatment modulated spatial memory impairment caused by TRPC1 depletion and the mechanisms may involve the modulation of EE on the expression of those dys-regulated proteins such as α-internexin and GMF-β in hippocampus.

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