The vast majority of ischemic stroke patients are unable to receive treatment with tissue plasminogen activator (tPA) within the drug's three-hour efficacy window, and there are no approved therapies that promote recovery of motor function after the damage is done. Researchers at the University of California, Los Angeles think they have a solution to the latter problem after having shownthat inhibitors of GABAA receptor increase functional recovery in mice when given several days post-stroke.1
A key next step will be honing the therapeutic window for GABAA receptor blockers, as the molecules have negative effects when given immediately following a stroke.
The brain houses two types of GABAA receptors with differing functions and structures. The synaptic (phasic) type regulates signaling between neurons. The extrasynaptic (tonic) type inhibits neuronal