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The neurotransmitter glutamate is released following ischemic brain damage, and its excitotoxic effects contribute greatly to the development of stroke. Because this release of glutamate occurs within minutes, therapeutic drugs targeting the restriction of glutamate-induced excitotoxicity must be administered quickly following ischemic onset. Here, we evaluate an alternative research approach examining the overexpression of glutamate transporter 1 (GLT1) to reduce infarction and improve behavioral deficits induced by stroke in a rat model of stroke. Recent studies verify the role of glutamate overflow in the pathogenesis of stroke. The experimental approach evaluated glutamate clearance, following ischemia-induced overflow where the GLT had been genetically manipulated to be overexpressed in the ischemic region. A viral vector-mediated gene transfer approach activated the overexpression of GLT1 to successfully reduce ischemia-induced glutamate overflow, decrease cell death, and improve behavioral recovery among animal models. These findings further support the role of glutamate in the pathogenesis of stroke and the upregulation of endogenous GLT1 as a promising approach to protect against the effects of ischemic brain damage caused by glutamate excitotoxicity. This study is a review article. Referred literature in this paper has been listed in the references part. The datasets supporting the conclusions of this article are available online by searching the PubMed. Some original points in this article come from the laboratory practice in our research centers and our experiences.

Reducing excitoxicity with glutamate transporter-1 to treat stroke