GABARAP is not essential for GABAA receptor targeting to the synapse

Authors

  • Gregory A. O'Sullivan,

    1. Department of Neurochemistry, Max-Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany
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  • Matthias Kneussel,

    1. Department of Neurochemistry, Max-Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany
    2. Center for Molecular Neurobiology (ZMNH), University of Hamburg, Falkenried 94, 20251 Hamburg, Germany
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  • Zvulun Elazar,

    1. Department of Biological Chemistry, Ullman Building, Weizmann Institute of Science, 76100 Rehovot, Israel
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  • Heinrich Betz

    1. Department of Neurochemistry, Max-Planck Institute for Brain Research, Deutschordenstrasse 46, 60528 Frankfurt, Germany
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Dr Heinrich Betz, as above.
E-mail: Neurochemie@mpih-frankfurt.mpg.de

Abstract

GABAA receptors (GABAARs) containing the γ2 subunit are thought to require the interacting protein GABARAP (GABAAR associated protein) for trafficking to the neuronal plasma membrane. In order to assess whether GABARAP is required for GABAA receptor accumulation at synaptic sites, we analysed a GABARAP knockout mouse. GABARAP deficient mice are phenotypically normal and do not show up-regulation of other GABARAP homologues. Also, the total number of GABAARs, as assessed by benzodiazepine binding, is unaffected by the loss of GABARAP. Immunocytochemistry of cortical sections showed no differences in the expression and punctate distribution of the γ2 subunit and the receptor anchoring protein gephyrin between GABARAP deficient and wild-type mice. Thus, GABARAP is not essential for trafficking γ2 subunit containing GABAARs to the neuronal plasma membrane or targeting them to inhibitory synapses.

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