Journal
ONCOTARGET
Volume 7, Issue 43, Pages 69337-69346Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12567
Keywords
TRPC1; basal ganglia; movement disorder; neuronal loss
Categories
Funding
- NSFC (the National Natural Science Foundation of China) [81673134, 81501213, 81571294]
- Guangdong Provincial Natural Science Foundation [2014A030313715, 2016A030313051]
- Guangdong Provincial Scheme of Science and Technology
- Shenzhen Special Fund Project on Strategic Emerging Industry Development [JCY20160428143433768, JCYJ20150529164656093, JCYJ20150529153646078]
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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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