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Vascular smooth muscle TRPC3 channels facilitate the inverse hemodynamic response during status epilepticus

Michael A Cozart1, Kevin D Phelan2, Hong Wu3

  • 1Department of Pharmacology and Toxicology, Little Rock, Arkansas, United States of America. macozart2@uams.edu.

Scientific Reports
|January 23, 2020
PubMed

Insights

Targeting TRPC3 channels in smooth muscle cells can improve cerebral blood flow during seizures. This study shows that blocking these channels reduces seizure duration and improves neurovascular coupling in status epilepticus.

Area of Science:

  • Neuroscience
  • Cardiovascular Biology
  • Genetics

Background:

  • Status epilepticus (SE) involves reduced cerebral blood flow (inverse hemodynamic response, IHR).
  • Canonical transient receptor potential 3 (TRPC3) channels in vascular smooth muscle cells (VSMCs) mediate vasoconstriction and are implicated in seizure propagation.
  • The role of cerebrovascular TRPC3 channels in SE-induced IHR remains unclear.

Purpose of the Study:

  • To investigate the contribution of TRPC3 channels in cerebral VSMCs to seizure-induced IHR.
  • To determine the effect of ablating VSMC-specific TRPC3 channels on neurovascular coupling and SE duration.

Main Methods:

  • Development of a smooth muscle-specific TRPC3 knockout (TRPC3smcKO) mouse model.
  • Simultaneous electroencephalogram (EEG) recordings and laser speckle contrast imaging (LSCI) to assess neurovascular coupling.
  • Quantification of cerebral blood flow changes and seizure activity.

Main Results:

  • Control mice exhibited variable IHRs with limited, uncorrelated cerebral blood flow increases during SE.
  • TRPC3smcKO mice demonstrated enhanced, less variable cerebral blood flow positively correlated with neuronal activity.
  • Genetic ablation of smooth muscle TRPC3 channels significantly shortened SE duration by eliminating a secondary seizure phase.

Conclusions:

  • TRPC3 channels in cerebral VSMCs contribute significantly to the IHR during SE.
  • Targeting VSMC TRPC3 channels represents a potential therapeutic strategy to mitigate SE progression by improving neurovascular coupling.

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