NDLI: Delayed $K^{+}$ clearance associated with aquaporin-4 mislocalization: Phenotypic defects in brains of α-syntrophin-null mice

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Delayed $K^{+}$ clearance associated with aquaporin-4 mislocalization: Phenotypic defects in brains of α-syntrophin-null mice

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Delayed $K^{+}$ clearance associated with aquaporin-4 mislocalization: Phenotypic defects in brains of α-syntrophin-null mice

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Williamson, Anne Nagelhus, Erlend A. Froehner, Stanley C. Palomba, Maria Adams, Marvin E. De Lanerolle, Nihal C. Agre, Peter Amiry-moghaddam, Mahmood Eid, Tore Ottersen, Ole P.
Description	Author Affiliation: Amiry-Moghaddam M ( Centre for Molecular Biology and Neuroscience, University of Oslo, 0317 Oslo, Norway.);
Abstract	Recovery from neuronal activation requires rapid clearance of potassium ions (K+) and restoration of osmotic equilibrium. The predominant water channel protein in brain, aquaporin-4 (AQP4), is concentrated in the astrocyte end-feet membranes adjacent to blood vessels in neocortex and cerebellum by association with alpha-syntrophin protein. Although AQP4 has been implicated in the pathogenesis of brain edema, its functions in normal brain physiology are uncertain. In this study, we used immunogold electron microscopy to compare hippocampus of WT and alpha-syntrophin-null mice (alpha-Syn-/-). We found that <10% of AQP4 immunogold labeling is retained in the perivascular astrocyte end-feet membranes of the alpha-Syn-/- mice, whereas labeling of the inwardly rectifying K+ channel, Kir4.1, is largely unchanged. Activity-dependent changes in K+ clearance were studied in hippocampal slices to test whether AQP4 and K+ channels work in concert to achieve isosmotic clearance of K+ after neuronal activation. Microelectrode recordings of extracellular K+ ([K+]o) from the target zones of Schaffer collaterals and perforant path were obtained after 5-, 10-, and 20-Hz orthodromic stimulations. K+ clearance was prolonged up to 2-fold in alpha-Syn-/- mice compared with WT mice. Furthermore, the intensity of hyperthermia-induced epileptic seizures was increased in approximately half of the alpha-Syn-/-mice. These studies lead us to propose that water flux through perivascular AQP4 is needed to sustain efficient removal of K+ after neuronal activation.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	23
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Brain Metabolism Membrane Proteins Physiology Muscle Proteins Potassium Animals Astrocytes Calcium-Binding Proteins Electrophysiology Epilepsy Hippocampus Immunohistochemistry Genetics Mice Mice, Inbred C57BL Mice, Transgenic Neurons Phenotype Potassium Channels, Inwardly Rectifying Seizures Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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