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Downregulation of the tumor suppressor, phosphatase and tensin homolog deleted on chromosome 10 (PTEN), is thought to be a novel neuroprotective strategy in ischemic stroke, but the underlying mechanisms remain unclear. In this study, we aimed to validate the use of PTEN regulation of gamma-aminobutyric acid subtype A receptors (GABA(A)Rs) as a molecular target for the treatment of ischemic stroke. Because suppression of GABA(A)Rs contributes to ischemic neuron death, describing the intracellular signaling that interacts with GABA(A)Rs in ischemic neurons would provide a molecular basis for novel stroke therapies.

Preservation of GABA A Receptor Function by PTEN Inhibition Protects Against Neuronal Death in Ischemic Stroke

Preservation of GABA _A Receptor Function by PTEN Inhibition Protects Against Neuronal Death in Ischemic Stroke