Oncotarget

Research Papers: Pathology:

Movement deficits and neuronal loss in basal ganglia in TRPC1 deficient mice

Kaiwu He, Fei Qi, Chunni Guo, Shuqin Zhan, Hua Xu, Jianjun Liu and Xifei Yang _

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Oncotarget. 2016; 7:69337-69346. https://doi.org/10.18632/oncotarget.12567

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Abstract

Kaiwu He1,2,*, Fei Qi3,*, Chunni Guo4, Shuqin Zhan5, Hua Xu1, Jianjun Liu2 and Xifei Yang2

1 College of Pharmacy, Jinan University, Guangzhou, China

2 Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China

3 Department of Respiratory Medicine, Chinese People’s Liberation Army General Hospital, Beijing, China

4 Department of Neurology, Shanghai First People’s Hospital Affiliated to Shanghai Jiaotong University, Shanghai, China

5 Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China

* These authors have contributed equally to this work

Correspondence to:

Xifei Yang, email:

Hua Xu, email:

Keywords: TRPC1; basal ganglia; movement disorder; neuronal loss; Pathology Section

Received: June 29, 2016 Accepted: October 03, 2016 Published: October 11, 2016

Abstract

Transient receptor potential cation (TRPC) channel proteins are abundantly expressed in brain. However, the functions of these TRPC proteins such as TRPC1 are largely unclear. In this study, we reported that TRPC1 deficiency caused movement disorder as measured by swimming test, modified open field test and sunflower seeds eating test. Immunofluorescent staining showed significant loss of both NeuN-positive cells and tyrosine hydroxylase (TH) -positive cells in the caudate putamen (CPu), the external globus pallidus (GPe), and the substantia nigra pars reticulata (SNr) in 5-month-old TRPC1 knockout mice (TRPC1-/-) compared to the wild type (WT) mice. TUNEL staining further revealed that TUNEL-positive cells were significantly increased in the CPu, GPe, and SNr of TRPC1-/- mice. Taken together, these data suggests that TRPC1 is involved in the control of motor function by inhibiting the apoptosis of neuronal cells of basal ganglia.


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