Reducing excessive GABA-mediated tonic inhibition promotes functional recovery after stroke
Andrew N. Clarkson,
Ben S. Huang,
Sarah E. MacIsaac,
Istvan Mody and
S. Thomas Carmichael ()
Additional contact information
Andrew N. Clarkson: The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA
Ben S. Huang: The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA
Sarah E. MacIsaac: The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA
Istvan Mody: The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA
S. Thomas Carmichael: The David Geffen School of Medicine at UCLA, 635 Charles Young Drive South, Los Angeles, California 90095, USA
Nature, 2010, vol. 468, issue 7321, 305-309
Abstract:
A target for boosting stroke recovery Stroke 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.
Date: 2010
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DOI: 10.1038/nature09511
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