Temporary loss of perivascular aquaporin-4 in neocortex after transient middle cerebral artery occlusion in mice

Aug 30, 2006Proceedings of the National Academy of Sciences of the United States of America

Temporary loss of water channels around blood vessels in the brain's thinking area after brief artery blockage in mice

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Abstract

Quantitative analysis reveals a loss of perivascular AQP4 in the striatal core after 24 hours of reperfusion following ischemic stroke.

Distinct patterns of AQP4 expression were observed in the ischemic striatum and neocortex during the reperfusion phase after middle cerebral artery occlusion.
The striatal core experienced a significant loss of perivascular AQP4 with no signs of recovery at 24 hours post-reperfusion.
The affected cortex showed a similar loss of perivascular AQP4, but there was a partial recovery noted by 72 hours of reperfusion.
Loss of perivascular AQP4 was linked to the disappearance of characteristic square lattice structures in the astrocyte membrane.
The cortical border zone exhibited a slight increase in perivascular AQP4 at 24 hours of reperfusion, contrasting with the central ischemic lesion.

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The aquaporin-4 (AQP4) pool in the perivascular astrocyte membranes has been shown to be critically involved in the formation and dissolution of brain edema. Cerebral edema is a major cause of morbidity and mortality in stroke. It is therefore essential to know whether the perivascular pool of AQP4 is up- or down-regulated after an ischemic insult, because such changes would determine the time course of edema formation. Here we demonstrate by quantitative immunogold cytochemistry that the ischemic striatum and neocortex show distinct patterns of AQP4 expression in the reperfusion phase after 90 min of middle cerebral artery occlusion. The striatal core displays a loss of perivascular AQP4 at 24 hr of reperfusion with no sign of subsequent recovery. The most affected part of the cortex also exhibits loss of perivascular AQP4. This loss is of magnitude similar to that of the striatal core, but it shows a partial recovery toward 72 hr of reperfusion. By freeze fracture we show that the loss of perivascular AQP4 is associated with the disappearance of the square lattices of particles that normally are distinct features of the perivascular astrocyte membrane. The cortical border zone differs from the central part of the ischemic lesion by showing no loss of perivascular AQP4 at 24 hr of reperfusion but rather a slight increase. These data indicate that the size of the AQP4 pool that controls the exchange of fluid between brain and blood during edema formation and dissolution is subject to large and region-specific changes in the reperfusion phase.

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Temporary loss of perivascular aquaporin-4 in neocortex after transient middle cerebral artery occlusion in mice

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