000143156 001__ 143156
000143156 005__ 20181228151102.0
000143156 022__ $$a0271-678X
000143156 02470 $$2PMID$$a11919508
000143156 0247_ $$2doi$$a10.1097/00004647-200204000-00001
000143156 037__ $$aARTICLE
000143156 245__ $$aAquaporins in brain: distribution, physiology, and pathophysiology
000143156 269__ $$a2002
000143156 260__ $$c2002
000143156 336__ $$aJournal Articles
000143156 520__ $$aWater homeostasis in the brain is of central physiologic and clinical importance. Neuronal activity and ion water homeostasis are inextricably coupled. For example, the clearance of K+ from areas of high neuronal activity is associated with a concomitant water flux. Furthermore, cerebral edema, a final common pathway of numerous neurologic diseases, including stroke, may rapidly become life threatening because of the rigid encasement of the brain. A water channel family, the aquaporins, facilitates water flux through the plasma membrane of many cell types. In rodent brain, several recent studies have demonstrated the presence of different types of aquaporins. Aquaporin 1 (AQP1) was detected on epithelial cells in the choroid plexus whereas AQP4, AQP5 and AQP9 were localized on astrocytes and ependymal cells. In rodent brain, AQP4 is present on astrocytic end-feet in contact with brain vessels, and AQP9 is found on astrocytic processes and cell bodies. In basal physiologic conditions, AQP4 and AQP9 appear to be implicated in brain homeostasis and in central plasma osmolarity regulation. Aquaporin 4 may also play a role in pathophysiologic conditions, as shown by the reduced edema formation observed after water intoxication and focal cerebral ischemia in AQP4-knockout mice. Furthermore, pathophysiologic conditions may modulate AQP4 and AQP9 expression. For example, AQP4 and AQP9 were shown to be upregulated after ischemia or after traumatic injuries. Taken together, these recent reports suggest that water homeostasis in the brain is maintained by regulatory processes that, by control of aquaporin expression and distribution, induce and organize water movements. Facilitation of these movements may contribute to the development of edema formation after acute cerebral insults such as ischemia or traumatic injury.
000143156 700__ $$aBadaut, Jérôme
000143156 700__ $$aLasbennes, François
000143156 700__ $$0243698$$g134990$$aMagistretti, Pierre J
000143156 700__ $$aRegli, Luca
000143156 773__ $$j22$$tJournal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism$$k4$$q367-78
000143156 909C0 $$xU11150$$0252265$$pLNDC
000143156 909CO $$qSV$$particle$$ooai:infoscience.tind.io:143156
000143156 937__ $$aLNDC-ARTICLE-2002-010
000143156 973__ $$rREVIEWED$$sPUBLISHED$$aOTHER
000143156 980__ $$aARTICLE