Abstract
The ability of transforming growth factor-β2 (TGFβ2) to directly regulate neuronal sensitivity to glutamate and N-methyl- d-aspartate (NMDA) excitotoxicity in rat cerebral cortical neurons was investigated. Mixed neuronal-glial cultures treated with TGFβ2 (1–10 ng/ml) exhibited a significant 25–50% increase in neuronal death compared to control cultures. TGFβ2 potentiation of this endogenous glutamate excitotoxicity was blocked by the selective NMDA receptor antagonist, 2-amino-5-phosphonovalerate. In addition, neuronal death induced by brief NMDA exposure in both mixed neuronal-glial and pure neuronal cultures was increased by TGFβ2 (1–30 ng/ml) with a similar dose-response curve. These findings indicate that TGFβ2, at physiologically relevant concentrations, potentiates NMDA receptor-mediated excitotoxicity and that this occurs independently of TGFβ2 effects on glia.
Published Version
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