Expression of TRPC3 in cortical lesions from patients with focal cortical dysplasia

Chao Liang1, Xin Chen2, Chun-Qing Zhang1

  • 1Epilepsy Research Center of PLA, Department of Neurosurgery, Xinqiao Hospital, Army Medical University (Third Military Medical University), Chongqing, 400037, PR China.

Neuroscience Letters
|March 6, 2020
PubMed

Insights

Transient receptor potential canonical channel 3 (TRPC3) is overexpressed in focal cortical dysplasia (FCD), a cause of intractable epilepsy. This suggests TRPC3 may contribute to seizure development in FCD patients.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Epilepsy Research

Background:

  • Focal cortical dysplasia (FCD) is a primary cause of medically intractable epilepsy.
  • Transient receptor potential canonical channel 3 (TRPC3) has been implicated in seizure occurrence.

Purpose of the Study:

  • To investigate the expression patterns of TRPC3 in different types of FCD.
  • To determine the cellular distribution of TRPC3 in FCD specimens.

Main Methods:

  • Western blotting to quantify TRPC3 protein levels.
  • Immunohistochemistry and immunofluorescence staining to visualize TRPC3 distribution.
  • Analysis of 45 FCD specimens and 12 autopsy control samples.

Main Results:

  • TRPC3 protein levels were significantly elevated in FCD samples compared to controls.
  • TRPC3 staining was prominent in malformed cells and microcolumns within FCD tissues.
  • TRPC3-positive cells frequently co-expressed glutamatergic and GABAergic markers.

Conclusions:

  • Overexpression and altered cellular localization of TRPC3 in FCD suggest its potential role in epileptogenesis.
  • TRPC3 may be a contributing factor to seizure generation in focal cortical dysplasia.

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