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一氧化氮可促进经红藻氨酸处理的大鼠的癫痫发作活动。

Nitric oxide promotes seizure activity in kainate-treated rats.

作者信息

Mülsch A, Busse R, Mordvintcev P I, Vanin A F, Nielsen E O, Scheel-Krüger J, Olesen S P

机构信息

Zentrum der Physiologie, Universität Frankfurt, Germany.

出版信息

Neuroreport. 1994 Nov 21;5(17):2325-8. doi: 10.1097/00001756-199411000-00029.

Abstract

L-Arginine-derived nitrogen monoxide (NO) formation was determined in different regions of the rat brain during kainate-induced seizures. NO was trapped in vivo as a paramagnetic mononitrosyl-iron diethyldithiocarbamate complex, the concentration of which was determined ex vivo by cryogenic electron spin resonance spectroscopy. Basal NO formation (0.3-0.8 nmol g-1 tissue 30 min-1) was detected in the brain of control rats. In kainate-injected rats NO formation was increased six-fold within 30-60 min in the amygdala/temporal cortex region, and up to 12-fold, though more slowly, in the remaining cortex. The kainate-elicited convulsions and NO formation were attenuated in animals pretreated with either 7-nitroindazole, a specific inhibitor of neuronal NO synthase, or diazepam. These findings identify NO as a proconvulsant mediator in kainate-evoked seizures.

摘要

在大鼠脑内不同区域,测定了在红藻氨酸诱导的癫痫发作期间由L-精氨酸衍生的一氧化氮(NO)的生成情况。NO在体内被捕获形成顺磁性二乙氨基二硫代甲酸盐单亚硝基铁络合物,其浓度通过低温电子自旋共振光谱法在体外测定。在对照大鼠脑中检测到基础NO生成(0.3 - 0.8 nmol g-1组织30 min-1)。在注射红藻氨酸的大鼠中,杏仁核/颞叶皮质区域内30 - 60分钟内NO生成增加了6倍,在其余皮质中增加了12倍,不过速度较慢。在用神经元型NO合酶的特异性抑制剂7-硝基吲唑或地西泮预处理的动物中,红藻氨酸引发的惊厥和NO生成均减弱。这些发现确定NO是红藻氨酸诱发癫痫发作中的一种促惊厥介质。

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