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

大脑包含两种细胞，一种是传递信息的神经细胞，另一种是神经细胞正常运作所必需的神经胶质细胞。两种主要的胶质细胞是星形胶质细胞和少突胶质细胞。少突胶质细胞形成髓鞘，髓鞘对神经信号的快速传递至关重要。少突胶质细胞在脑瘫中不能正常发育，在脱髓鞘疾病多发性硬化症中丢失，导致这些疾病的衰弱临床症状。同时，在信号传递的过程中，神经会释放出化学物质。抹去?星形胶质细胞。星形胶质细胞这些保护功能的破坏会导致癫痫发作和神经死亡，这种情况发生在癫痫、中风和脑损伤中。我们的工作帮助证明了一种叫做Kir4.1的特殊胶质蛋白对胶质细胞的特殊功能是绝对必要的。在人类中，Kir4.1基因与一般癫痫易感性有关，Kir4.1基因的缺失会导致髓磷脂的缺失和星形胶质细胞保护功能的破坏。我们对Kir4.1调节神经胶质细胞功能的机制进行了基础研究，这将为癫痫易感性、损伤和白质病理提供信息。

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.