Aquaporin and blood brain barrier

Abstract

Large water fluxes continuously take place between the different compartments of the brain as well as between the brain parenchyma and the blood or cerebrospinal fluid.Disturbances in this well-regulated water homeostasis may have deleterious effects on brain function and may be fatal in cases where water accumulates in the brain following pathologies such as ischemia, haemorrhage, or brain trauma.The molecular pathways by which water molecules cross the blood brain barrier are not well-understood, although the discovery of Aquaporin 4 (AQP4) in the brain improved the understanding of some of these transport processes, particularly under pathological conditions.

Keywords: Central nervous system; aquaporin.; blood brain barrier.

Fig. (1)

Double immunolabeling of AQP4 (red) and glial fibrillary acidic protein (GFAP) (green) in cortex. AQP4 immunolabeling reveals that the entire network of vessels, including capillaries, is covered by astrocytic processes, albeit GFAP negative. Smaller vessels and capillaries are mostly GFAP negative but display intense labeling against the astrocyte-specific channel AQP4. The AQP4 labeling reveals continuous coverage by astrocytic end feet. Figures from Simard et al. [38], reprinted with permission of Society of Neuroscience.

Fig. (2)

Proposed mechanism of AQP4 involvement in edema fluid formation. (A) In cytotoxic edema, the entry of excess fluid into the brain parenchyma is AQP4 dependent, because edema fluid flows from the vascular compartment, through intact BBB and AQP4-rich astrocyte foot processes, and accumulates primarily in astrocytes. (B) In vasogenic edema, water accumulation is AQP4-independent because the BBB is leaky, permitting the entry of plasma fluid directly into the brain ECS circumventing astrocyte foot processes.