Mode of action of taurine as a neuroprotector

被引:145
作者
Wu, H
Jin, Y
Wei, JN
Jin, H
Sha, D
Wu, JY [1 ]
机构
[1] Florida Atlantic Univ, Dept Biomed Sci, Boca Raton, FL 33431 USA
[2] Univ Kansas, Dept Pharmaceut Chem, Lawrence, KS 66045 USA
关键词
taurine; glutamate; excitotoxicity; calcium channel; amino acid receptor; neuroprotection;
D O I
10.1016/j.brainres.2005.01.058
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Previously, it has been shown that taurine exerts its protective function against glutamate-induced neuronal excitotoxicity through its action in reducing glutamate-induced elevation of intracellular free calcium, [Ca2+](i). Here, we report the mechanism underlying the effect of taurine in reducing [Ca2+](i). We found that taurine inhibited glutamate-induced calcium influx through L-, P/Q-, N-type voltage-gated calcium channels (VGCCs) and NMDA receptor calcium channel. Surprisingly, taurine had no effect on calcium influx through NMDA receptor calcium channel when cultured neurons were treated with NMDA in Mg2+-free medium. Since taurine was found to prevent glutamate-induced membrane depolarization, we propose that taurine protects neurons against glutamate excitotoxicity by preventing glutamate-induced membrane depolarization, probably through its effect in opening of chloride channels and, therefore, preventing the glutamate-induced increase in calcium influx and other downstream events. (c) 2005 Elsevier B.V. All rights reserved.
引用
收藏
页码:123 / 131
页数:9
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