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    GABAA receptor availability is not altered in adults with autism spectrum disorder or in mouse models

    Access Status
    Fulltext not available
    Authors
    Horder, J.
    Andersson, M.
    Mendez, M.
    Singh, N.
    Tangen, A.
    Lundberg, J.
    Gee, A.
    Halldin, C.
    Veronese, M.
    Bolte, Sven
    Farde, L.
    Sementa, T.
    Cash, D.
    Higgins, K.
    Spain, D.
    Turkheimer, F.
    Mick, I.
    Selvaraj, S.
    Nutt, D.
    Lingford-Hughes, A.
    Howes, O.
    Murphy, D.
    Borg, J.
    Date
    2018
    Type
    Journal Article
    
    Metadata
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    Citation
    Horder, J. and Andersson, M. and Mendez, M. and Singh, N. and Tangen, A. and Lundberg, J. and Gee, A. et al. 2018. GABAA receptor availability is not altered in adults with autism spectrum disorder or in mouse models. Science Translational Medicine. 10 (461): eaam8434.
    Source Title
    Science Translational Medicine
    DOI
    10.1126/scitranslmed.aam8434
    ISSN
    1946-6234
    School
    School of Occ Therapy, Social Work and Speech Path
    URI
    http://hdl.handle.net/20.500.11937/72449
    Collection
    • Curtin Research Publications
    Abstract

    Copyright © 2018 The Authors, some rights reserved. Preliminary studies have suggested that -aminobutyric acid type A (GABAA) receptors, and potentially the GABAA 5 subtype, are deficient in autism spectrum disorder (ASD). However, prior studies have been confounded by the effects of medications, and these studies did not compare findings across different species. We measured both total GABAA and GABAA 5 receptor availability in two positron emission tomography imaging studies. We used the tracer [11C]flumazenil in 15 adults with ASD and in 15 control individuals without ASD and the tracer [11C]Ro15-4513 in 12 adults with ASD and in 16 control individuals without ASD. All participants were free of medications. We also performed autoradiography, using the same tracers, in three mouse models of ASD: the Cntnap2 knockout mouse, the Shank3 knockout mouse, and mice carrying a 16p11.2 deletion. We found no differences in GABAA receptor or GABAA 5 subunit availability in any brain region of adults with ASD compared to those without ASD. There were no differences in GABAA receptor or GABAA 5 subunit availability in any of the three mouse models. However, adults with ASD did display altered performance on a GABA-sensitive perceptual task. Our data suggest that GABAA receptor availability may be normal in adults with ASD, although GABA signaling may be functionally impaired.

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