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首页> 外文期刊>Brain research >Role of kinin B1 and B2 receptors in the development of pilocarpine model of epilepsy.
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Role of kinin B1 and B2 receptors in the development of pilocarpine model of epilepsy.

机译:激肽B1和B2受体在毛细支芸香碱癫痫模型发展中的作用。

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The tissue sclerosis found in epilepsy of limbic origin is characterized by shrunken gliotic hippocampus, granule cell loss in the dentate gyrus and extensive pyramidal cell loss in Ammon's horn. Evidence has indicated that sprouting of dentate granule cell axons into the inner molecular layer of the dentate gyrus is related to hyperexcitability. Trying to understand the role of kinin B1 and B2 receptors in the physiopathology of temporal lobe epilepsy (TLE), the present work was delineated to study the development of the epilepsy model induced by pilocarpine in B1 and B2 knockout mice (B1KO and B2KO, respectively). Behavior parameters, cell death and mossy fiber sprouting were analyzed. B1KO mice showed increased latency for the first seizure, associated to a decreased frequency of spontaneous seizures, when compared with wild-type mice. In addition, B1KO mice showed less cell death in all hippocampal formation associated to a reduced grade of mossy fiber sprouting. Furthermore, B2KO mice presented minor duration of the silent period and an increased frequency of spontaneous seizures, when compared with wild-type mice. B2KO and their control lineage showed similar pattern of cell death in the hippocampus, which was very intense when compared with saline-treated animals. The mossy fiber sprouting was also increased in B2KO mice, when compared to wild-type mice and saline-treated animals. Taken together, these data suggest a deleterious effect for kinin B1 receptor and a protective effect for kinin B2 receptor during the development of the temporal lobe epilepsy.
机译:在边缘性癫痫发作中发现的组织硬化的特征是萎缩的胶质海马体,齿状回中的颗粒细胞损失和阿蒙角中的大量锥体细胞损失。有证据表明,齿状颗粒细胞轴突发芽到齿状回的内分子层与过度兴奋性有关。为了了解激肽B1和B2受体在颞叶癫痫(TLE)的生理病理学中的作用,本工作旨在研究毛果芸香碱在B1和B2敲除小鼠(分别为B1KO和B2KO)中诱发癫痫模型的发展)。分析行为参数,细胞死亡和苔藓纤维发芽。与野生型小鼠相比,B1KO小鼠的首次癫痫发作潜伏期延长,与自发癫痫发作频率降低相关。此外,B1KO小鼠在所有海马结构中显示出更少的细胞死亡,这与苔藓纤维发芽程度降低有关。此外,与野生型小鼠相比,B2KO小鼠的沉默期较短,自发性癫痫发作的频率增加。 B2KO及其对照谱系在海马中显示出相似的细胞死亡模式,与经盐水处理的动物相比,该模式非常强烈。与野生型小鼠和盐水处理的动物相比,B2KO小鼠的苔藓纤维发芽也增加了。在一起,这些数据表明在颞叶癫痫的发展过程中,激肽B1受体的有害作用和激肽B2受体的保护作用。

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