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Neuronal gap junctions play a role in the secondary neuronal death following controlled cortical impact

Andrei B Belousov1, Yongfu Wang, Ji-Hoon Song

  • 1Department of Molecular and Integrative Physiology, University of Kansas Medical Center, Kansas City, KS 66160, USA. abelousov@kumc.edu

Neuroscience Letters
|July 12, 2012
PubMed

Insights

Neuronal gap junctions contribute to secondary brain damage after traumatic brain injury (TBI). Blocking these junctions or related glutamate receptors reduced neuronal death in a mouse TBI model, highlighting a potential therapeutic target.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Neurology

Background:

  • Excessive glutamate release and receptor overactivation cause secondary neuronal death after CNS injury.
  • Neuronal gap junctions are implicated in excitotoxicity and ischemia-induced neuronal death.

Purpose of the Study:

  • To investigate the role of neuronal gap junctions in secondary neuronal death following controlled cortical impact (CCI), a model of traumatic brain injury (TBI).

Main Methods:

  • Controlled cortical impact (CCI) in adult mice to model TBI.
  • Fluoro-Jade B staining to quantify neuronal death.
  • Administration of mefloquine (neuronal gap junction blocker) and LY341495 (group II metabotropic glutamate receptor antagonist).
  • Analysis in wild-type and connexin 36 knockout mice.

Main Results:

  • Substantial neuronal death was observed in brain regions outside the injury core 24 hours post-CCI.
  • Striatal neuronal death was significantly reduced by mefloquine treatment in wild-type mice.
  • Neuronal death was also reduced in connexin 36 knockout mice and with group II metabotropic glutamate receptor inactivation.

Conclusions:

  • Neuronal gap junctions play a critical role in mediating secondary neuronal death after CCI-induced TBI.
  • Targeting neuronal gap junctions or associated glutamate receptors may offer a therapeutic strategy for TBI.

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