Ionic Imbalance Causes Cell Damage in Stroke

Researchers from the brain research center at the University of British Columbia Hospital (UBC, Vancouver, Canada) and the Vancouver Coastal Health Research Institute (VCHRI, Canada) found that during strokes in animal models, brain cell membranes were disrupted at the site of gap junction hemichannels--paired junctions that allow molecules and ions to flow between cells across the intercellular space. The neuronal excitotoxicity during stroke caused activation of unidentified large-conductance channels, leading to swelling and calcium dysregulation. These hemichannel openings contributed to profound ionic dysregulation, disrupting levels of critical brain cell ingredients such as calcium and potassium, and leading to rapid cell death.

The next step in the investigation will be to determine the cause of the hemichannel malfunction. Scientists can then develop a compound to block brain cell hemichannels from opening, and perhaps therapies for stroke patients may be available within five to 10 years. The findings were published in the May 12, 2006, edition of Science.

"We've known for 40 years about chemicals flowing out of cells after stroke, but nobody knew the exact process--so we went looking for the death channel. And we found it,” said lead author Roger Thompson, a UBC psychiatry post-doctoral fellow.

Until now, scientists believed the disruption to occur at the site of glutamate channels, one of the brain's most abundant chemical messengers. However, therapeutic strategies targeted at glutamate channels have failed to prevent brain cell death.



Related Links:
University of British Columbia
Vancouver Coastal Health Research Institute