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异常表达的 stathmin 1 在难治性颞叶癫痫患者脑组织和大鼠模型中。

Abnormal expression of stathmin 1 in brain tissue of patients with intractable temporal lobe epilepsy and a rat model.

机构信息

Department of Neurology, the First Affiliated Hospital, Chongqing Medical University, Chongqing 400016, China.

出版信息

Synapse. 2012 Sep;66(9):781-91. doi: 10.1002/syn.21567. Epub 2012 May 23.

DOI:10.1002/syn.21567
PMID:22535533
Abstract

Microtubule dynamics have been shown to contribute to neurite outgrowth, branching, and guidance. Stathmin 1 is a potent microtubule-destabilizing factor that is involved in the regulation of microtubule dynamics and plays an essential role in neurite elongation and synaptic plasticity. Here, we investigate the expression of stathmin 1 in the brain tissues of patients with intractable temporal lobe epilepsy (TLE) and experimental animals using immunohistochemistry, immunofluorescence and western blotting. We obtained 32 temporal neocortex tissue samples from patients with intractable TLE and 12 histologically normal temporal lobe tissues as controls. In addition, 48 Sprague Dawley rats were randomly divided into six groups, including one control group and five groups with epilepsy induced by lithium chloride-pilocarpine. Hippocampal and temporal lobe tissues were obtained from control and epileptic rats on Days 1, 7, 14, 30, and 60 after kindling. Stathmin 1 was mainly expressed in the neuronal membrane and cytoplasm in the human controls, and its expression levels were significantly higher in patients with intractable TLE. Moreover, stathmin 1 was also expressed in the neurons of both the control and the experimental rats. Stathmin 1 expression was decreased in the experimental animals from 1 to 14 days postseizure and then significantly increased at Days 30 and 60 compared with the control group. Many protruding neuronal processes were observed in the TLE patients and in the chronic stage epileptic rats. These data suggest that stathmin 1 may participate in the abnormal network reorganization of synapses and contribute to the pathogenesis of TLE.

摘要

微管动力学已被证明有助于轴突生长、分支和导向。Stathmin 1 是一种有效的微管解聚因子,参与微管动力学的调节,在轴突伸长和突触可塑性中发挥重要作用。在这里,我们使用免疫组织化学、免疫荧光和 Western blot 技术研究了难治性颞叶癫痫(TLE)患者和实验动物脑组织中 stathmin 1 的表达。我们从难治性 TLE 患者中获得了 32 个颞叶新皮质组织样本,并以 12 个组织学正常的颞叶组织作为对照。此外,48 只 Sprague Dawley 大鼠随机分为 6 组,包括 1 组对照组和 5 组匹罗卡品诱导的癫痫组。在点燃后第 1、7、14、30 和 60 天,从对照组和癫痫大鼠中获取海马和颞叶组织。Stathmin 1 主要在人类对照组的神经元膜和细胞质中表达,其表达水平在难治性 TLE 患者中显著升高。此外,stathmin 1 也在对照和实验大鼠的神经元中表达。与对照组相比,在癫痫发作后 1 至 14 天,实验动物的 stathmin 1 表达减少,然后在第 30 和 60 天显著增加。在 TLE 患者和慢性期癫痫大鼠中观察到许多突出的神经元突起。这些数据表明,stathmin 1 可能参与突触的异常网络重组,并有助于 TLE 的发病机制。

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