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首页> 外文期刊>The European Journal of Neuroscience >Persistent reduction of hippocampal glutamine synthetase expression after status epilepticus in immature rats
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Persistent reduction of hippocampal glutamine synthetase expression after status epilepticus in immature rats

机译：未成熟大鼠癫痫持续状态后海马谷氨酰胺合成酶的表达持续降低

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摘要

Mesiotemporal sclerosis (MTS), the most frequent form of drug-resistant temporal lobe epilepsy, often develops after an initial precipitating injury affecting the immature brain. To analyse early processes in epileptogenesis we used the juvenile pilocarpine model to study status epilepticus (SE)-induced changes in expression of key components in the glutamate-glutamine cycle, known to be affected in MTS patients. SE was induced by Li+/pilocarpine injection in 21-day-old rats. At 2-19weeks after SE hippocampal protein expression was analysed by immunohistochemistry and neuron damage by FluoroJade staining. Spontaneous seizures occurred in at least 44% of animals 15-18weeks after SE. As expected in this model, we did not observe loss of principal hippocampal neurons. Neuron damage was most pronounced in the hilus, where we also detected progressive loss of parvalbumin-positive GABAergic interneurons. Hilar neuron loss (or end-folium sclerosis), a common feature in patients with MTS, was accompanied by a progressively decreased glutamine synthetase (GS)-immunoreactivity from 2 (-15%) to 19weeks (-33.5%) after SE. Immunoreactivity for excitatory amino-acid transporters, vesicular glutamate transporter 1 and glial fibrillary acidic protein was unaffected. Our data show that SE elicited in 21-day-old rats induces a progressive reduction in hilar GS expression without affecting other key components of the glutamate-glutamine cycle. Reduced expression of glial enzyme GS was first detected 2weeks after SE, and thus clearly before spontaneous recurrent seizures occurred. These results support the hypothesis that reduced GS expression is an early event in the development of hippocampal sclerosis in MTS patients and emphasize the importance of astrocytes in early epileptogenesis.
机译：颞叶硬皮病（MTS）是耐药性颞叶癫痫病最常见的形式，通常在最初的未成熟先天性损伤引起后发展。为了分析癫痫发生的早期过程，我们使用了青少年毛果芸香碱模型研究了癫痫持续状态（SE）诱导的谷氨酸-谷氨酰胺循环中关键成分表达的变化，已知MTS患者会受到影响。在21日龄大鼠中，Li + /毛果芸香碱注射液可诱发SE。 SE后2-19周，通过免疫组织化学分析海马蛋白表达，并通过FluoroJade染色分析神经元损伤。 SE后15-18周，至少有44％的动物发生自发性癫痫发作。如该模型中所预期的，我们没有观察到主要海马神经元的丢失。神经元的损伤在希尔斯（Hilus）中最为明显，在那我们还检测到小白蛋白阳性的GABA能中间神经元逐渐丢失。肺门神经元丢失（或叶端硬化）是MTS患者的常见特征，伴有谷氨酰胺合成酶（GS）免疫活性从SE后2周（-15％）逐渐降低至19周（-33.5％）。兴奋性氨基酸转运蛋白，囊状谷氨酸转运蛋白1和神经胶质原纤维酸性蛋白的免疫反应性不受影响。我们的数据表明，在21天大的大鼠中诱发的SE引起肺门GS表达的逐渐降低，而不会影响谷氨酸-谷氨酰胺循环的其他关键成分。 SE后2周首次检测到神经胶质酶GS的表达降低，因此很明显在自发性复发性癫痫发作之前。这些结果支持以下假设：GS表达降低是MTS患者海马硬化发展中的早期事件，并强调了星形胶质细胞在早期癫痫发生中的重要性。

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