According to the researchers, hemichannels, which were previously found to cause cell death after a stroke, may also cause epileptic seizures that occur following head trauma or a stroke.
A hemichannel is a channel that can form in nerve cells which allows chemical ions to pass through. And the new findings will enable the researchers to focus on new treatments that block these channels.
"The glutamate receptor that is linked to cell death following a stroke also triggers opening of hemichannels. Therefore both the stroke itself or the glutamate released by a stroke can open hemichannels and cause cell death or epileptic seizures," said UBC Psychiatry Prof. Brian MacVicar, who is a member of the Brain Research Centre at UBC and VCH Research Institute.
By testing the effect of glutamate at levels less than those reached during stroke the researchers found that more moderate activation of glutamate receptors opens hemichannels and causes seizure but does not produce cell death associated with stroke.
Glutamate is one of the brain's most abundant chemical messengers. Gap junctions are connections that allow molecules and ions, to flow between cells. Junctions are composed of two hemichannels that bridge intercellular space.
When epileptic seizures occur, hemichannels open unexpectedly near the synapses, disrupting the normal electrical activity of the brain leading to seizures.
"We found that blocking hemichannels reduced the epilepsy-like discharges," said Roger Thompson, a former UBC Psychiatry post-doctoral Fellow.
MacVicar added: "With these results we are confident that the discovery of safe blockers of hemichannels will provide a new therapy in the treatment to reduce cell loss and seizures that are caused by stroke.
"The next step will be to develop a compound to block brain cell hemichannels from opening. Therapies for epilepsy patients who have suffered a stroke or head trauma may be available within five to 10 years."
The study is published in Science.