| Aquaporin-4-dependent K+ and water transport modeled in brain extracellular space following neuroexcitation. | |
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MedLine Citation:
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PMID: 23277478 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Potassium (K(+)) ions released into brain extracellular space (ECS) during neuroexcitation are efficiently taken up by astrocytes. Deletion of astrocyte water channel aquaporin-4 (AQP4) in mice alters neuroexcitation by reducing ECS [K(+)] accumulation and slowing K(+) reuptake. These effects could involve AQP4-dependent: (a) K(+) permeability, (b) resting ECS volume, (c) ECS contraction during K(+) reuptake, and (d) diffusion-limited water/K(+) transport coupling. To investigate the role of these mechanisms, we compared experimental data to predictions of a model of K(+) and water uptake into astrocytes after neuronal release of K(+) into the ECS. The model computed the kinetics of ECS [K(+)] and volume, with input parameters including initial ECS volume, astrocyte K(+) conductance and water permeability, and diffusion in astrocyte cytoplasm. Numerical methods were developed to compute transport and diffusion for a nonstationary astrocyte-ECS interface. The modeling showed that mechanisms b-d, together, can predict experimentally observed impairment in K(+) reuptake from the ECS in AQP4 deficiency, as well as altered K(+) accumulation in the ECS after neuroexcitation, provided that astrocyte water permeability is sufficiently reduced in AQP4 deficiency and that solute diffusion in astrocyte cytoplasm is sufficiently low. The modeling thus provides a potential explanation for AQP4-dependent K(+)/water coupling in the ECS without requiring AQP4-dependent astrocyte K(+) permeability. Our model links the physical and ion/water transport properties of brain cells with the dynamics of neuroexcitation, and supports the conclusion that reduced AQP4-dependent water transport is responsible for defective neuroexcitation in AQP4 deficiency. |
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Authors:
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Byung-Ju Jin; Hua Zhang; Devin K Binder; A S Verkman |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of general physiology Volume: 141 ISSN: 1540-7748 ISO Abbreviation: J. Gen. Physiol. Publication Date: 2013 Jan |
Date Detail:
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Created Date: 2013-01-01 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 2985110R Medline TA: J Gen Physiol Country: United States |
Other Details:
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Languages: eng Pagination: 119-32 Citation Subset: IM |
Affiliation:
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Department of Medicine and 2 Department of Physiology, University of California, San Francisco, San Francisco, CA 94143. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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