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The importance of immunohistochemical analyses in evaluating the phenotype of Kv channel knockout mice.

Abstract

To gain insights into the phenotype of voltage-gated potassium (Kv)1.1 and Kv4.2 knockout mice, we used immunohistochemistry to analyze the expression of component principal or α subunits and auxiliary subunits of neuronal Kv channels in knockout mouse brains. Genetic ablation of the Kv1.1 α subunit did not result in compensatory changes in the expression levels or subcellular distribution of related ion channel subunits in hippocampal medial perforant path and mossy fiber nerve terminals, where high levels of Kv1.1 are normally expressed. Genetic ablation of the Kv4.2 α subunit did not result in altered neuronal cytoarchitecture of the hippocampus. Although Kv4.2 knockout mice did not exhibit compensatory changes in the expression levels or subcellular distribution of the related Kv4.3 α subunit, we found dramatic decreases in the cellular and subcellular expression of specific Kv channel interacting proteins (KChIPs) that reflected their degree of association and colocalization with Kv4.2 in wild-type mouse and rat brains. These studies highlight the insights that can be gained by performing detailed immunohistochemical analyses of Kv channel knockout mouse brains.

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  • Authors

    Menegola M, Clark E, Trimmer JS

    Institution

    Departments of Neurobiology, Physiology and Behavior Physiology and Membrane Biology, University of California-Davis, One Shields Avenue, Davis, CA 95616-8519, U.S.A.

    Source

    Epilepsia 53 Suppl 1: 2012 Jun pg 142-9

    MeSH

    Animals
    Blotting, Western
    Brain Chemistry
    Calcium-Binding Protein, Vitamin D-Dependent
    Coloring Agents
    Fluorescent Antibody Technique
    Immunohistochemistry
    Kv Channel-Interacting Proteins
    Kv1.1 Potassium Channel
    Mice
    Mice, Knockout
    Mossy Fibers, Hippocampal
    Potassium Channels, Voltage-Gated
    Presynaptic Terminals
    Shal Potassium Channels
    Up-Regulation

    Pub Type(s)

    Journal Article
    Research Support, N.I.H., Extramural
    Research Support, Non-U.S. Gov't

    Language

    eng

    PubMed ID

    22612819