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Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke
Published Web Location
https://doi.org/10.1038/nature09511Abstract
A target for boosting stroke recoveryStroke is a leading cause of disability because of the brain's limited capacity for recovery. The functional recovery that does occur derives in part from the transfer of brain function to the tissue bordering the stroke site. A study in a mouse model shows that stroke reduces excitation in neurons adjacent to the stroke site by impairing transport of GABA, leading to a build-up of this inhibitory neurotransmitter. Genetic or pharmacological blockade of extrasynaptic GABAA receptors improves behavioural recovery. Critically, the treatment remains successful when there is a delay between stroke and therapy. This work identifies novel pharmacological targets for neural recovery after stroke and possibly other brain injuries.
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