| Literature DB >> 26280213 |
Zhenle Zang1, Song Li1, Wei Zhang1, Xin Chen1, Dahai Zheng1, Haifeng Shu1,2, Wei Guo1, Bangyun Zhao1, Kaifeng Shen1, YuJia Wei1, Xin Zheng1, Shiyong Liu3, Hui Yang4.
Abstract
Focal cortical dysplasia (FCD) is known as a common cause of chronic refractory epilepsy, but the underlying mechanisms of the factors that lead to FCD-related epilepsy are unclear. Previous studies have shown that canonical transient receptor potential channels (TRPCs) might be involved in the process of epileptogenesis. Canonical transient receptor potential channel 1 (TRPC1), which is ubiquitously expressed in the brain, has been shown to be involved in epileptiform bust firing in knockout mice. In this study, we examined the expression of TRPC1 in FCD type Ia (FCDIa), FCD type IIa (FCDIIa), and FCD type IIb (FCDIIb) surgical specimens from patients and age-matched autopsy control samples. Real-time quantitative PCR and western blotting indicated that TRPC1 mRNA and protein levels were increased in FCDIa, FCDIIa, and FCDIIb samples compared to control samples. Immunohistochemistry results revealed that TRPC1 was mainly distributed in microcolumns, dysmorphic neurons, and balloon cells. Further double immunofluorescent staining showed that TRPC1 was co-localized with glutamatergic and GABAergic markers. Taken together, our results demonstrate that the overexpression and specific cellular location of TRPC1 might be related to the epileptogenesis of FCD.Entities:
Keywords: Canonical transient receptor potential channels type-1; Epilepsy; Focal cortical dysplasia
Mesh:
Substances:
Year: 2015 PMID: 26280213 DOI: 10.1007/s12031-015-0615-5
Source DB: PubMed Journal: J Mol Neurosci ISSN: 0895-8696 Impact factor: 3.444