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一氧化氮可诱导纹状体切片中依赖钙的[3H]多巴胺释放。

Nitric oxide induces calcium-dependent [3H]dopamine release from striatal slices.

作者信息

Lonart G, Cassels K L, Johnson K M

机构信息

Department of Pharmacology and Toxicology, University of Texas Medical Branch, Galveston 77555-1031.

出版信息

J Neurosci Res. 1993 Jun 1;35(2):192-8. doi: 10.1002/jnr.490350210.

DOI:10.1002/jnr.490350210
PMID:8100588
Abstract

Hydroxylamine (0.01-30 mM), a nitric oxide (NO) generator, produced a concentration-dependent release of [3H]dopamine ([3H]DA) from rat striatal slices. Hemoglobin (10 microM), a NO scavenger, reduced basal [3H]DA release and blocked hydroxylamine (100 microM)-stimulated [3H]DA efflux. Tetrodotoxin (0.5 microM) had no significant effect. Sodium cyanide was used as a model compound to test the possibility that NO acted through blockade of mitochondrial electron transport. Calcium-free experimental buffer (1 mM EGTA) reduced basal release and the hydroxylamine response, while sodium cyanide-induced release did not change under these experimental conditions. Cadmium (200 microM), a non-selective inhibitor of voltage-dependent calcium channels, reduced the hydroxylamine response by 69%. Methylene blue (10 microM), an inhibitor of guanylate cyclase, produced a 3-fold increase in the basal release but had no significant effect on the hydroxylamine response. These data suggest that NO induces calcium-dependent [3H]DA release from the striatum via a mechanism which is independent of blockade of electron transport or activation of guanylate cyclase.

摘要

羟胺(0.01 - 30 mM),一种一氧化氮(NO)生成剂,可使大鼠纹状体切片中[3H]多巴胺([3H]DA)呈浓度依赖性释放。血红蛋白(10 microM),一种NO清除剂,可减少基础[3H]DA释放,并阻断羟胺(100 microM)刺激的[3H]DA流出。河豚毒素(0.5 microM)无显著作用。氰化钠用作模型化合物,以测试NO是否通过阻断线粒体电子传递起作用。无钙实验缓冲液(1 mM乙二醇双乙醚二胺四乙酸)可减少基础释放和羟胺反应,而在这些实验条件下,氰化钠诱导的释放没有变化。镉(200 microM),一种电压依赖性钙通道的非选择性抑制剂,可使羟胺反应降低69%。亚甲蓝(10 microM),一种鸟苷酸环化酶抑制剂,可使基础释放增加3倍,但对羟胺反应无显著影响。这些数据表明,NO通过一种独立于电子传递阻断或鸟苷酸环化酶激活的机制,诱导纹状体中钙依赖性[3H]DA释放。

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