A central puzzle in our understanding of aquaporin 4 (AQP4) is the observation that paravascular astrocytic end-feet express abundant AQP4, whereas the cerebral microvessels they abut express tight junctions and no known aquaporins [1]. Much of previous research exploring the role of AQP4 in water transport has focused on the tripartite synapse. This model places pre- and postsynaptic neuronal, and perisynaptic astrocyte processes as the central point initiating fluid movement [2]. Smith et al. suggest that osmotic gradients provide the dominant driving force for water movement, as a result of the large ion fluctuations that accompany neuronal activity, in small extracellular space (ECS) dimensions (Figure 1A) [3].

中文翻译：

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过滤脑水肿的浑水

我们对水通道蛋白 4 (AQP4) 理解的一个核心难题是观察到血管旁星形胶质细胞末端足部表达丰富的 AQP4，而与它们相邻的大脑微血管表达紧密连接且没有已知的水通道蛋白 [1]。以前探索 AQP4 在水运输中的作用的许多研究都集中在三方突触上。该模型将突触前和突触后神经元以及突触周围星形胶质细胞过程作为启动流体运动的中心点 [2]。史密斯等人。表明渗透梯度为水运动提供了主要驱动力，作为伴随神经元活动的大离子波动的结果，在小的细胞外空间 (ECS) 尺寸（图 1A）[3]。