Regulation of the cell surface expression of chloride transporters during epileptogenesis.
Regulation of the cell surface expression of chloride transporters during epileptogenesis.
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DOI：
10.1016/j.neulet.2016.06.042
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发表时间：
2016-08-15
影响因子：
2.5
通讯作者：
González MI
中科院分区：
文献类型：
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作者：
González MI
这个过程通常被称为癫痫发生是指分子和细胞变化的级联反应，这些变化改变了大脑，使其变得过度兴奋，并能够产生反复自发性癫痫发作。不幸的是，我们对癫痫发生过程中影响大脑的分子变化的理解仍然不完整。最近的证据表明，阳离子氯转运体（CCCs）功能障碍可能是导致癫痫发生过程中观察到的抑制性神经传递缺陷的因素之一。本研究分析了癫痫发生和慢性癫痫期间CCC的细胞表面表达，以评估CCC从质膜的丢失是否可能导致过度兴奋。CCCs的质膜表达的变化主要是在致痫期的早期阶段检测到的，这表明CCCs的功能障碍可能有助于先前检测到的氯离子梯度的改变。总之，这里提出的研究结果表明，CCC的质膜水平的异常调节可能有助于GABA能神经传递的免疫，CCC功能障碍可能与自发性癫痫发作的最初出现有关。
The process is commonly known as epileptogenesis refers to the cascade of molecular and cellular changes that transform the brain to make it hyperexcitable and capable of generate recurrent spontaneous seizures. Unfortunately, our understanding of the molecular changes that affect the brain during epileptogenesis remains incomplete. Recent evidence suggests that dysfunction of cation-chloride transporters (CCCs) might be one of the factors that contribute to the deficits in inhibitory neurotransmission observed during epileptogenesis. This study analyzed the cell surface expression of CCCs during epileptogenesis and during chronic epilepsy to evaluate if a loss of CCCs from the plasma membrane might contribute to hyperexcitability. Alterations in the plasma membrane expression of CCCs were mostly detected during the early phase of the epileptogenic period, suggesting that dysfunction of CCCs might contribute to the alterations in the chloride gradient previously detected. Together, the findings presented here suggest that aberrant regulation of the plasma membrane levels of CCCs might contribute to the impartment of GABAergic neurotransmission and that CCCs dysfunction might be relevant for the initial appearance of spontaneous seizures.