Badaut Jérôme, Lasbennes François, Magistretti Pierre J, Regli Luca
Département de Neurochirurgie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
J Cereb Blood Flow Metab. 2002 Apr;22(4):367-78. doi: 10.1097/00004647-200204000-00001.
Water homeostasis in the brain is of central physiologic and clinical importance. Neuronal activity and ion water homeostasis are inextricably coupled. For example, the clearance of K+ from areas of high neuronal activity is associated with a concomitant water flux. Furthermore, cerebral edema, a final common pathway of numerous neurologic diseases, including stroke, may rapidly become life threatening because of the rigid encasement of the brain. A water channel family, the aquaporins, facilitates water flux through the plasma membrane of many cell types. In rodent brain, several recent studies have demonstrated the presence of different types of aquaporins. Aquaporin 1 (AQP1) was detected on epithelial cells in the choroid plexus whereas AQP4, AQP5 and AQP9 were localized on astrocytes and ependymal cells. In rodent brain, AQP4 is present on astrocytic end-feet in contact with brain vessels, and AQP9 is found on astrocytic processes and cell bodies. In basal physiologic conditions, AQP4 and AQP9 appear to be implicated in brain homeostasis and in central plasma osmolarity regulation. Aquaporin 4 may also play a role in pathophysiologic conditions, as shown by the reduced edema formation observed after water intoxication and focal cerebral ischemia in AQP4-knockout mice. Furthermore, pathophysiologic conditions may modulate AQP4 and AQP9 expression. For example, AQP4 and AQP9 were shown to be upregulated after ischemia or after traumatic injuries. Taken together, these recent reports suggest that water homeostasis in the brain is maintained by regulatory processes that, by control of aquaporin expression and distribution, induce and organize water movements. Facilitation of these movements may contribute to the development of edema formation after acute cerebral insults such as ischemia or traumatic injury.
大脑中的水平衡具有核心的生理和临床重要性。神经元活动与离子及水平衡紧密相连。例如，从神经元高活动区域清除钾离子与伴随的水通量相关。此外，脑水肿是包括中风在内的众多神经系统疾病的最终共同通路，由于大脑的坚硬包裹，可能迅速危及生命。水通道蛋白家族促进水通过多种细胞类型的质膜流动。在啮齿动物大脑中，最近的几项研究已证明存在不同类型的水通道蛋白。水通道蛋白1（AQP1）在脉络丛上皮细胞中被检测到，而水通道蛋白4、水通道蛋白5和水通道蛋白9定位于星形胶质细胞和室管膜细胞。在啮齿动物大脑中，水通道蛋白4存在于与脑血管接触的星形胶质细胞终足上，水通道蛋白9存在于星形胶质细胞突起和细胞体上。在基础生理条件下，水通道蛋白4和水通道蛋白9似乎参与大脑稳态和中央血浆渗透压调节。水通道蛋白4在病理生理条件下可能也起作用，如在水通道蛋白4基因敲除小鼠中，水中毒和局灶性脑缺血后观察到水肿形成减少所表明的那样。此外，病理生理条件可能调节水通道蛋白4和水通道蛋白9的表达。例如，水通道蛋白4和水通道蛋白9在缺血或创伤性损伤后被证明上调。综上所述，这些最新报道表明，大脑中的水平衡通过调节过程得以维持，这些过程通过控制水通道蛋白的表达和分布来诱导和组织水的流动。促进这些流动可能导致急性脑损伤如缺血或创伤性损伤后水肿形成的发展。
