After effects gradient along stroke7/27/2023 Genetically lowering the number of α5 or δ-subunit-containing GABA ARs responsible for tonic inhibition also proved beneficial for post-stroke recovery, consistent with the therapeutic potential of diminishing extrasynaptic GABA AR function. This treatment produced an early and sustained recovery of motor function. To counteract the heightened inhibition, we administered in vivo a benzodiazepine inverse agonist specific for the α5-subunit-containing extrasynaptic GABA ARs at a delay after stroke. This increased tonic inhibition is mediated by extrasynaptic GABA A receptors (GABA ARs) and is caused by an impairment in GABA transporter (GAT-3/4) function. Here we show that after a stroke in mice, tonic neuronal inhibition is increased in the peri-infarct zone. Thus, understanding the neuronal properties constraining this plasticity is important to developing new treatments. The brain region adjacent to stroke damage, the peri-infarct zone, is critical for rehabilitation, as it exhibits heightened neuroplasticity, allowing sensorimotor functions to re-map from damaged areas 1 – 3. Stroke is a leading cause of disability but no pharmacological therapy is currently available for promoting recovery.
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