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首页> 外文期刊>Epilepsia: Journal of the International League against Epilepsy >Glutamine synthetase becomes nitrated and its activity is reduced during repetitive seizure activity in the pentylentetrazole model of epilepsy.
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Glutamine synthetase becomes nitrated and its activity is reduced during repetitive seizure activity in the pentylentetrazole model of epilepsy.

机译：在癫痫的戊戊四唑模型的反复发作中，谷氨酰胺合成酶被硝化并且其活性降低。

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PURPOSE: The astrocyte-specific glutamine synthetase (GS) plays a key role in glutamate recycling and Gamma-aminobutyric acid (GABA) metabolism. Changes in the expression or activity of GS have been proposed to contribute to epileptogenesis. The mechanisms or how and where GS may contribute to epilepsy is still a matter of discussion. Here we asked the question whether brain regions, which show an astrocytic stress response respond with alterations of GS. METHODS: Biochemical and histological alterations of GS, HSP-27, and GFAP were studied after pentylenetetrazole-induced repetitive epileptic seizures (PIRS) in rats using a topographical quantification of the GS-immunoreactivity (GSIR) in relation to the focal heat shock response (HSR). Saline-treated rats served as controls and rats treated by the GS-inhibitor, L-methionine-sulfoximine (MSO) served as a positive control. RESULTS: No changes in the amount of GSIR and GS-protein occurred during PIRS. A significant reduction of GSIR was observed by histochemistry (in situ) and in native (nonheated) protein extracts of MSO-treated rats. In rats affected by PIRS, GS-activity showed a significant, region-specific reduction in association with a nitration of the enzyme. DISCUSSION: These results show that neither PIRS nor GS-inhibition reduced the amount of GS protein, but that MSO interferes with antibody binding to native GS. PIRS resulted in a focal increase of astrocytic stress response, whereas MSO caused a widespread, homogeneous astrocytic HSR independent from quantitative changes of GS content. In rats with PIRS the regions showing a strong glial HSR, respond with reduced GS-activity and GS-nitration, which all together are clear indicators of a nitrosative stress response.
机译：目的：星形胶质细胞特异性谷氨酰胺合成酶（GS）在谷氨酸循环和γ-氨基丁酸（GABA）代谢中起关键作用。已经提出GS的表达或活性的变化有助于癫痫发生。 GS可能促成癫痫的机制或方式和作用仍在讨论中。在这里，我们提出了一个问题，即显示星形细胞应激反应的大脑区域是否会随着GS的变化而做出反应。方法：使用GS免疫反应性（GSIR）相对于局灶性热休克反应（GSIR）的地形图量化，研究了戊四氮诱导的大鼠重复性癫痫发作（PIRS）后GS，HSP-27和GFAP的生化和组织学改变。高铁）。用盐水处理的大鼠作为对照，用GS抑制剂L-蛋氨酸-亚磺酰亚胺（MSO）处理的大鼠作为阳性对照。结果：PIRS期间GSIR和GS蛋白的含量没有变化。通过组织化学（原位）和MSO处理的大鼠的天然（非加热）蛋白提取物观察到GSIR显着降低。在受到PIRS影响的大鼠中，GS活性与酶的硝化作用相关，显示出明显的区域特异性降低。讨论：这些结果表明，PIRS和GS抑制均不能降低GS蛋白的量，但是MSO会干扰抗体与天然GS的结合。 PIRS导致了星形胶质细胞应激反应的局部增加，而MSO则引起了广泛，均匀的星形胶质HSR，而与GS含量的定量变化无关。在患有PIRS的大鼠中，表现出强烈神经胶质HSR的区域具有降低的GS活性和GS硝化反应，所有这些共同是亚硝化应激反应的明确指标。

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