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首页> 外文期刊>Biochimica et biophysica acta. Biomembranes >Role of astrocyte connexin hemichannels in cortical spreading depression
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Role of astrocyte connexin hemichannels in cortical spreading depression

机译：星形胶质细胞connexin血管在皮质蔓延抑郁症的作用

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Abstract Cortical spreading depression (CSD) is an intriguing phenomenon consisting of massive slow brain depolarizations that affects neurons and glial cells. It has been recognized since 1944, but its pathogenesis has only been uncovered during the last decade. Acute brain injuries can be further complicated by CSD in >50% of severe cases. This phenomenon is repetitive and produces a metabolic overload that increments secondary damage. Propagation of CSD is known to be linked to excitotoxicity, but the mechanisms associated with its initiation remain less understood. It has been shown that CSD can be initiated by increases in extracellular [K + ] ([K + ] e ), and animal models use high [K + ] e to promote CSD. Connexin hemichannel activity increases due to high [K + ] e and low extracellular [Ca 2+ ], conditions that occur after brain injury. Moreover, glial cell gap junction channels are fundamental in controlling extracellular medium composition, particularly in maintaining normal extracellular glutamate and K + concentrations through “spatial buffering”. However, the role of astrocytic gap junctions under tissue stress can change to damage spread in the acute damage zone whereas the reduced communication in adjacent zone would reduce cell dead propagation. Here, we review the main findings associated with CSD, and discuss the possible involvement of astrocytic connexin-based channels in secondary damage propagation. This article is part of a Special Issue entitled: Gap Junction Proteins edited by Jean Claude Herve. Highlights ? Cortical spreading depression (CSD) consisting of massive slow brain depolarizations that affects neurons and glial cells. ? CSD complicates the evolution of acute brain injuries and probably are the origin of aura migraine. ? CSD initiation remains unknown but is associated to increase in extracellular [K + ], and glutamate excitotoxicity. ? Astrocytes control the extracellular medium composition. ? Connexin-based channels have a key role in the astroglia spatial buffering and could be associated to CSD initiation.
机译：摘要皮质扩散抑郁症（CSD）是一种有趣现象，其由影响神经元和神经胶质细胞的大规模慢脑去氧组成。自1944年以来已被认可，但其发病机制在过去十年中仅被揭露。急性脑损伤可通过CSD进一步复杂化> 50％的严重病例。这种现象是重复性的，并产生代谢过载，使次要损坏增加。已知CSD的繁殖与兴奋毒性有关，但与其启动相关的机制仍然不太了解。已经表明，CSD可以通过细胞外[k +]（[k +] e）的增加来引发，并且动物模型使用高[k +] e来促进CSD。 Connexin血管笼活性由于高[K +] E和低细胞外[Ca 2+]，脑损伤后发生的条件增加。此外，胶质电池间隙结通道在控制细胞外介质组合物中是基础的，特别是通过“空间缓冲”保持正常细胞外谷氨酸和K +浓度。然而，星形胶质间隙连接在组织应激下的作用可以改变急性损伤区的损伤，而相邻区域的连续交际降低会降低细胞死亡。在这里，我们审查了与CSD相关的主要发现，并讨论了星形胶质Connexin基通道可能参与二次损伤传播。本文是题为的特殊问题的一部分：Jean Claude Herve编辑的Gap Junction蛋白。强调 ？皮质扩散抑郁（CSD）由影响神经元和胶质细胞的巨大慢脑去偏振组成。还CSD使急性脑损伤的演变复杂化，可能是偏头痛的起源。还CSD启动仍然未知，但与细胞外[k +]的增加有关，以及谷氨酸兴奋毒性增加。还星形胶质细胞控制细胞外培养基组成。还基于Connexin的频道在Astroglia空间缓冲中具有关键作用，并且可以与CSD启动相关联。

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