Aquaporins in brain: distribution, physiology, and pathophysiology

Détails

ID Serval
serval:BIB_17B919339BEC
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Institution
Titre
Aquaporins in brain: distribution, physiology, and pathophysiology
Périodique
Journal of Cerebral Blood Flow and Metabolism
Auteur⸱e⸱s
Badaut  J., Lasbennes  F., Magistretti  P. J., Regli  L.
ISSN
0271-678X
Statut éditorial
Publié
Date de publication
04/2002
Peer-reviewed
Oui
Volume
22
Numéro
4
Pages
367-78
Notes
Journal Article Research Support, Non-U.S. Gov't Review --- Old month value: Apr
Résumé
Water 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.
Mots-clé
Animals Aquaporins/chemistry/*metabolism Brain/cytology/*metabolism/physiopathology Cerebrospinal Fluid/metabolism Homeostasis Humans Models, Neurological Osmolar Concentration Water/*metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/01/2008 15:22
Dernière modification de la notice
20/08/2019 13:47
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