Our Laboratory has pursued the hypothesis that traumatic brain edema ispredominantly cellular and recent supportive evidence has been obtainedindicating a non-extracellular route for sodium and water enteringbrain. The aim of this study was to investigate if astrocytic endfeetare involved in this passage, using a potent activator of Protein KinaseC (phorbol ester) to modify and closing the Aquaporin 4 (AQP4), a waterchannel specific for astrocytic endfoot.Anaesthetized Sprague-Dawley rats were subjected to anintracerebroventricular bolus of phorbol ester (50 pmol/4 mul) orvehicle, in the right hemisphere and after 30 minutes they were exposedto the well-established cortical contusion model (3 mm depth at 6 m/sec)on the same side. After trauma, they were subjected to 5 hours of drugcontinuous infusion, then sacrificed. Water content measurements forboth right (injured) and left (uninjured) hemispheres were calculatedusing the wet weight/dry weight technique.Results of these experiments showed a significant decrease in watercontent in injured phorbol treated animals, underlying that AQP4regulation plays an important role in brain edema following stroke, andsupporting the concept of cellular formation for edema via astrocyticfoot processes.
Modulation of aquaporin-4 water transport in a model of TBI
Amorini;
2003-01-01
Abstract
Our Laboratory has pursued the hypothesis that traumatic brain edema ispredominantly cellular and recent supportive evidence has been obtainedindicating a non-extracellular route for sodium and water enteringbrain. The aim of this study was to investigate if astrocytic endfeetare involved in this passage, using a potent activator of Protein KinaseC (phorbol ester) to modify and closing the Aquaporin 4 (AQP4), a waterchannel specific for astrocytic endfoot.Anaesthetized Sprague-Dawley rats were subjected to anintracerebroventricular bolus of phorbol ester (50 pmol/4 mul) orvehicle, in the right hemisphere and after 30 minutes they were exposedto the well-established cortical contusion model (3 mm depth at 6 m/sec)on the same side. After trauma, they were subjected to 5 hours of drugcontinuous infusion, then sacrificed. Water content measurements forboth right (injured) and left (uninjured) hemispheres were calculatedusing the wet weight/dry weight technique.Results of these experiments showed a significant decrease in watercontent in injured phorbol treated animals, underlying that AQP4regulation plays an important role in brain edema following stroke, andsupporting the concept of cellular formation for edema via astrocyticfoot processes.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
