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Morphological and functional alterations of astrocytes following experimentally induced epilepsy.

机译：实验诱导的癫痫后星形胶质细胞的形态和功能改变。

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摘要

The mammalian central nervous system is comprised of a collection of cell types that include a variety of neuronal, glial, and blood vessel epithelial cells. The coordinated function of these cell types sustains neurotransmission and normal brain function. During the pathology of epilepsy, normal brain function is perturbed, resulting in spontaneous seizure activity. Historically, epilepsy research has focused mainly on the dysfunction of neuronal cell types. More recently, non-neuronal cell types have become implicated in the disease progression of epilepsy as well as other neurological disorders. The glial cells, and especially astrocytes, have gained the greatest attention. Once thought of merely as passive support cells, astrocytes are now known to be active participants of neurotransmission in the brain, thus making their study during epileptogenesis vital to better understanding the concerted series of events that leads to seizure activity in the epileptic brain.;Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy (TLE) we show multiple morphological and functional alterations of reactive astrocytes. One week following SE we observed pronounced astrogliosis accompanied by the increased expression of glial fibrillary acid protein, increased gap junction coupling accompanied by the dramatic increase of Cx43 expression, and the intact buffering ability of important extracellular constituents like potassium and glutamate. Furthermore, reactive hippocampal astrocytes begin to express specific kainate receptor (KAR) subunits following SE, as measured by immunohistochemistry and colocalization analysis. In the CA1 region of the hippocampus, GluK1, GluK2/3, GluK4 and GluK5 subunit expression was observed in GFAP positive astrocytes during the latent period 1 week following SE. At 8 weeks following SE, a time point when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits retained elevated expression at significant levels. KAR subunit expression in astrocytes appears to be restricted to the hippocampus and surrounding cortex. The immunohistochemistry results were corroborated using Western blotting on enriched astroglial fractions isolated from hippocampus. GluK4 receptor subunit expression was shown to be significantly increased in animals that experienced SE compared to age matched control animals.;While some of the alterations observed in astrocytes during the latent period might serve as a compensatory mechanism to reduce hyperexcitability, the potential expression of functioning KARs, in conjunction with astrogliosis, may contribute substantially to hyperexcitability, synchronization, and seizure generation in TLE.
机译：哺乳动物的中枢神经系统由一系列细胞类型组成，其中包括多种神经元，神经胶质细胞和血管上皮细胞。这些细胞类型的协调功能维持神经传递和正常的脑功能。在癫痫病的病理过程中，正常的脑功能受到干扰，导致自发性癫痫发作活动。历史上，癫痫研究主要集中在神经细胞类型的功能障碍。最近，非神经元细胞类型与癫痫以及其他神经系统疾病的疾病进展有关。胶质细胞，尤其是星形胶质细胞受到了最大的关注。曾经被认为只是被动支持细胞的星形胶质细胞现在被认为是大脑神经传递的活跃参与者，因此使它们在癫痫发生过程中的研究对于更好地了解导致癫痫脑癫痫发作的一系列事件至关重要。颞叶癫痫（TLE）的化学惊厥性癫痫持续状态（SE）模型，我们显示了反应性星形胶质细胞的多种形态和功能改变。 SE后一个星期，我们观察到明显的星形胶质变，伴有神经胶质纤维酸性蛋白表达增加，间隙连接偶联增加，Cx43表达急剧增加以及重要的细胞外成分（如钾和谷氨酸）的完整缓冲能力。此外，反应性海马星形胶质细胞在SE后开始表达特定的红藻氨酸受体（KAR）亚基，如通过免疫组织化学和共定位分析所测量的。在SE后1周的潜伏期中，在GFAP阳性星形胶质细胞中观察到海马CA1区的GluK1，GluK2 / 3，GluK4和GluK5亚基表达。 SE后8周，即自发的行为性癫痫发作发生的时间点，GluK1和GluK5亚基以显着水平保留了升高的表达。星形胶质细胞中的KAR亚基表达似乎仅限于海马和周围皮层。免疫组织化学结果使用Western印迹法从海马中富集的星形胶质细胞组分中得到证实。与年龄匹配的对照组动物相比，在经历SE的动物中GluK4受体亚基的表达明显增加。;尽管在潜伏期星形胶质细胞中观察到的某些改变可能是减少过度兴奋性的补偿机制，但功能的潜在表达KAR与星形胶质增生相关，可能会极大地促进TLE的过度兴奋，同步和癫痫发作。

著录项

  • 作者

    Vargas, Jay R.;

  • 作者单位

    The University of Utah.;

  • 授予单位 The University of Utah.;
  • 学科 Biology Neuroscience.;Health Sciences Pharmacology.;Biology Cell.
  • 学位 Ph.D.
  • 年度 2011
  • 页码 114 p.
  • 总页数 114
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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