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Expression Patterns of TRPC1 in Cortical Lesions from Patients with Focal Cortical Dysplasia. | LitMetric

Expression Patterns of TRPC1 in Cortical Lesions from Patients with Focal Cortical Dysplasia.

J Mol Neurosci

Department of Neurosurgery, Xinqiao Hospital, Third Military Medical University, 183 Xinqiao Main Street, Shapingba District, Chongqing, 400037, China.

Published: October 2015

AI Article Synopsis

  • Focal cortical dysplasia (FCD) is a common cause of chronic refractory epilepsy, but the exact mechanisms that lead to epilepsy from FCD are not well understood.
  • This study investigated the role of canonical transient receptor potential channel 1 (TRPC1) in different types of FCD surgical specimens, finding increased levels of TRPC1 mRNA and protein compared to control samples.
  • The results suggest that TRPC1 is not only overexpressed in FCD tissues but also specifically localized in key neuronal structures, indicating its potential involvement in the development of epilepsy related to FCD.

Article 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.

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Source
http://dx.doi.org/10.1007/s12031-015-0615-5DOI Listing

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