VOLTAGE-DEPENDENT CALCIUM-CHANNEL INVOLVEMENT IN NMDA-INDUCED ACTIVATION OF NOS

被引：11

作者：

ALAGARSAMY, S ^{[1
]}

JOHNSON, KM ^{[1
]}

机构：

[1] UNIV TEXAS, MED BRANCH, DEPT PHARMACOL & TOXICOL, GALVESTON, TX 77555 USA

来源：

NEUROREPORT | 1995年 / 6卷 / 16期

关键词：

L-METHYL-D-ASPARTATE (NMDA); GLUTAMATE; P-TYPE CALCIUM CHANNEL; AGA IVA TOXIN; CORTEX; RECEPTOR BINDING;

D O I：

10.1097/00001756-199511000-00035

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

WE have previously shown that N-methyl-D-aspartate (NMDA) increases nitric oxide synthase (NOS) activity in rat frontal cortex; however, the actual mechanism of this activation has not been addressed. Tetrodotoxin (TTX; 0.05 mu M) inhibited NMDA-activated NOS, suggesting that TTX-sensitive Na+ channels are interposed between the NMDA receptors and the NOS cellular compartment, The NMDA response was also blocked by voltage-dependent Ca2+ channel (VDCC) blockers including Cd2+, Co2+, funnel web spider toxin (FIX) and omega-Aga IVa, but not by nifedipine or omega-conotoxin. These data suggest that Ca2+ flux through P- and/or Q-type VDCC subsequent to NMDA-induced depolarization may be at least as important for NOS activation as Ca2+ entry through the NMDA receptor.

引用

页码：2250 / 2254

页数：5

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