Exposure of cultured cerebellar neurons to terfenadine prevented the N- methyl-D-aspartate (NMDA) receptor-mediated early appearance (30 min) of toxicity signs induced by the voltage sensitive sodium channel (VSSC) activator veratridine. Delayed neurotoxicity by veratridine (24 h) occurring independently from NMDA receptor activation was also prevented by terfenadine. Terfenadine did not protect from excitotoxicity following direct exposure of neurons to glutamate. Our results suggest that terfenadine may modulate endogenous glutamate release following activation of VSSCs.
Terfenadine prevents NMDA receptor-dependent and -independent toxicity following sodium channel activation / Diaz-Trelles, R.; Novelli, A.; Puia, G.; Fernandez-Sanchez, M. T.. - In: BRAIN RESEARCH. - ISSN 0006-8993. - 842:2(1999), pp. 478-481. [10.1016/S0006-8993(99)01828-4]
Terfenadine prevents NMDA receptor-dependent and -independent toxicity following sodium channel activation
Puia G.;
1999
Abstract
Exposure of cultured cerebellar neurons to terfenadine prevented the N- methyl-D-aspartate (NMDA) receptor-mediated early appearance (30 min) of toxicity signs induced by the voltage sensitive sodium channel (VSSC) activator veratridine. Delayed neurotoxicity by veratridine (24 h) occurring independently from NMDA receptor activation was also prevented by terfenadine. Terfenadine did not protect from excitotoxicity following direct exposure of neurons to glutamate. Our results suggest that terfenadine may modulate endogenous glutamate release following activation of VSSCs.
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