BLOCKADE OF RETINAL NMDA RECEPTORS BY SODIUM-NITROPRUSSIDE IS PROBABLY DUE TO NITRIC-OXIDE FORMATION

被引：24

作者：

UJIHARA, H

AKAIKE, A

TAMURA, Y

YOKOTA, T

SASA, M

KASHII, S

HONDA, Y

机构：

[1] FUKUYAMA UNIV,FAC PHARM & PHARMACEUT SCI,DEPT NEUROPHARMACOL,FUKUYAMA 72902,JAPAN

[2] YAMAGUCHI UNIV,SCH MED,DEPT PHARMACOL,UBE,YAMAGUCHI 755,JAPAN

[3] HIROSHIMA UNIV,SCH MED,DEPT PHARMACOL,HIROSHIMA 734,JAPAN

[4] KYOTO UNIV,FAC MED,DEPT OPHTHALMOL,KYOTO 606,JAPAN

来源：

JAPANESE JOURNAL OF PHARMACOLOGY | 1993年 / 61卷 / 04期

关键词：

NITROPRUSSIDE; N-METHYL-D-ASPARTATE (NMDA); RETINA;

D O I：

10.1254/jjp.61.375

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Effects of a nitric oxide (NO)-producing agent, sodium nitroprusside, on N-methyl-D-aspartate (NMDA) receptor activation in the cultured retinal neurons of rats were examined. NMDA in a Mg2+-free medium evoked inward currents at the resting membrane potential. Inward currents were also evoked by kainate. Sodium nitroprusside markedly reduced the NMDA-induced currents without affecting those induced by kainate. These results suggest the possible existence of a negative feed back system of NO which serves to regulate the activation of NMDA receptors in retinal neurons.

引用

页码：375 / 377

页数：3

共 10 条

[1]

AKAIKE A, 1992, JAPAN J PHARM S1, V58

[2] EXCITOTOXINS - A POSSIBLE NEW MECHANISM FOR THE PATHOGENESIS OF ISCHEMIC RETINAL DAMAGE [J].