Terfenadine prevents NMDA receptor-dependent and -independent toxicity following sodium channel activation

被引：13

作者：

Díaz-Trelles, R

Novelli, A

Puia, G

Fernández-Sánchez, MT ^{[1
]}

机构：

[1] Univ Oviedo, Fac Med, Dept Biochem & Mol Biol, E-33071 Oviedo, Spain

[2] Univ Oviedo, Dept Psychol, Fac Psychol, Oviedo, Spain

[3] Univ Modena, Dept Pharmaceut Sci, I-41100 Modena, Italy

来源：

BRAIN RESEARCH | 1999年 / 842卷 / 02期

关键词：

glutamate release; excitotoxicity; terfenadine;

D O I：

10.1016/S0006-8993(99)01828-4

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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. (C) 1999 Elsevier Science B.V. All rights reserved.

引用

页码：478 / 481

页数：4

共 17 条

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