Critical role for the inwardly rectifying potassium channel Kir4.1 in astrocyte and oligodendrocyte functions

大脑包含两种细胞，传递信息的神经和神经胶质细胞，神经胶质细胞是神经细胞正常运作所必需的。两种主要的神经胶质细胞是星形胶质细胞和少突胶质细胞。少突胶质细胞形成对神经信号的快速传递至关重要的髓鞘。少突胶质细胞在脑瘫中不能正常发育，并且在脱髓鞘疾病多发性硬化中丢失，导致这些疾病的衰弱临床体征。此外，在信号传输过程中，神经释放的化学物质是什么？擦干净了吗由星形胶质细胞组成。星形胶质细胞的这些保护功能的破坏导致癫痫发作和神经死亡，其发生在癫痫、中风和脑损伤中。我们的工作帮助表明，一种名为Kir4.1的特定胶质蛋白对胶质细胞的特殊功能至关重要。在人类中，Kir4.1基因与全身性癫痫易感性有关，Kir4.1的缺失导致髓鞘的缺失和星形胶质细胞保护功能的破坏。我们的研究是对Kir4.1调节神经胶质细胞功能的机制的基础研究，这将为癫痫易感性、损伤和白色病变提供信息。

The brain contains two kinds of cell, nerves that transmit information, and glial cells, which are essential for nerve cells to function correctly. The two main glial cells are astrocytes and oligodendrocytes. Oligodendrocytes form the myelin sheaths that are critical for rapid transmission of nerve signals. Oligodendrocytes do not develop properly in cerebral palsy and are lost in the demyelinating disease multiple sclerosis, resulting in the debilitating clinical signs of these diseases. Also, during transmission of signals nerves release chemicals which are ?mopped up? up by astrocytes. Disruption of these protective functions of astrocytes results in seizures and nerve death, which occur in epilepsy, stroke, and brain injury. Our work has helped show that a specific glial protein called Kir4.1 is absolutely essential for the specialised functions of glia. In humans, the Kir4.1 gene is linked to general seizure susceptibility, and loss of Kir4.1 causes the loss of myelin and disruption of astrocyte protective functions. Ours is fundamental research into the mechanisms by which Kir4.1 regulate glial cell functions, which will inform on seizure susceptibility, injury, and white matter pathology.