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Start Over Author "Puia, G" Journal brain research
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3. Terfenadine prevents NMDA receptor-dependent and -independent toxicity following sodium channel activation.

Author

Díaz-Trelles R, Novelli A, Puia G, and Fernández-Sánchez MT

Subjects
Animals, Cell Survival drug effects, Cells, Cultured, Dizocilpine Maleate pharmacology, Glutamic Acid pharmacology, Neurons cytology, Neurons drug effects, Pyrilamine pharmacology, Rats, Receptors, N-Methyl-D-Aspartate antagonists & inhibitors, Saxitoxin pharmacology, Sodium Channels drug effects, Tetrodotoxin pharmacology, Cerebellum physiology, Neurons physiology, Receptors, N-Methyl-D-Aspartate physiology, Sodium Channels physiology, Terfenadine pharmacology, Veratridine toxicity
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.

Published
1999
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