Aquaporin-4 and epilepsy

Authors

  • Devin K. Binder,

    Corresponding author
    1. Center for Glial-Neuronal Interactions, Division of Biomedical Sciences, University of California, Riverside, California
    • Center for Glial-Neuronal Interactions, Division of Biomedical Sciences, 1247 Webber Hall, University of California, Riverside, Riverside, CA 92521-0121
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  • Erlend A. Nagelhus,

    1. Centre for Molecular Biology and Neuroscience (CMBN), Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo, 0318 Oslo, Norway
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  • Ole Petter Ottersen

    1. Centre for Molecular Biology and Neuroscience (CMBN), Centre for Molecular Medicine Norway (NCMM), Nordic EMBL Partnership, University of Oslo, 0318 Oslo, Norway
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Abstract

Recent studies have implicated glial cells in modulation of synaptic transmission, so it is plausible that glial cells may have a functional role in the hyperexcitability characteristic of epilepsy. Indeed, alterations in distinct astrocyte membrane channels, receptors, and transporters have all been associated with the epileptic state. This review focuses on the potential roles of the glial water channel aquaporin-4 (AQP4) in modulation of brain excitability and in epilepsy. We will review studies of mice lacking AQP4 (Aqp4−/− mice) or α-syntrophin (an AQP4 anchoring protein) and discuss the available human studies demonstrating alterations of AQP4 in human epilepsy tissue specimens. We will conclude with new studies of AQP4 regulation and discuss the potential role of AQP4 in the development of epilepsy (epileptogenesis). While many questions remain unanswered, the available data indicate that AQP4 and its molecular partners may represent important new therapeutic targets. © 2012 Wiley Periodicals, Inc.

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