title: Movement deficits and neuronal loss in basal ganglia in TRPC1 deficient mice.
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.
authors.affiliation: College of Pharmacy, Jinan University, Guangzhou, China.|Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
authors.forename: Kaiwu
authors.initials: K
authors.lastname: He
authors.affiliation: Department of Respiratory Medicine, Chinese People's Liberation Army General Hospital, Beijing, China.
authors.forename: Fei
authors.initials: F
authors.lastname: Qi
authors.affiliation: Department of Neurology, ShanghaiFirst People's HospitalAffiliated toShanghai Jiaotong University, Shanghai, China.
authors.forename: Chunni
authors.initials: C
authors.lastname: Guo
authors.affiliation: Department of Neurology, Xuanwu Hospital of Capital Medical University, Beijing, China.
authors.forename: Shuqin
authors.initials: S
authors.lastname: Zhan
authors.affiliation: College of Pharmacy, Jinan University, Guangzhou, China.
authors.forename: Hua
authors.initials: H
authors.lastname: Xu
authors.affiliation: Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
authors.forename: Jianjun
authors.initials: J
authors.lastname: Liu
authors.affiliation: Key Laboratory of Modern Toxicology of Shenzhen, Shenzhen Center for Disease Control and Prevention, Shenzhen, China.
authors.forename: Xifei
authors.initials: X
authors.lastname: Yang
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000235:genetics; D001479:Basal Ganglia / Q000378:metabolism*; D002470:Cell Survival / Q000235:genetics; D018345:Mice, Knockout; D009043:Motor Activity / Q000235:genetics; D009069:Movement Disorders / Q000235:genetics* / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D050052:TRPC Cation Channels / Q000172:deficiency / Q000235:genetics*
chemical_list: D050052:TRPC Cation Channels; C096351:transient receptor potential cation channel, subfamily C, member 1
keywords: TRPC1; basal ganglia; movement disorder; neuronal loss; Pathology Section