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dc.contributor.authorHorder, J.
dc.contributor.authorAndersson, M.
dc.contributor.authorMendez, M.
dc.contributor.authorSingh, N.
dc.contributor.authorTangen, A.
dc.contributor.authorLundberg, J.
dc.contributor.authorGee, A.
dc.contributor.authorHalldin, C.
dc.contributor.authorVeronese, M.
dc.contributor.authorBolte, Sven
dc.contributor.authorFarde, L.
dc.contributor.authorSementa, T.
dc.contributor.authorCash, D.
dc.contributor.authorHiggins, K.
dc.contributor.authorSpain, D.
dc.contributor.authorTurkheimer, F.
dc.contributor.authorMick, I.
dc.contributor.authorSelvaraj, S.
dc.contributor.authorNutt, D.
dc.contributor.authorLingford-Hughes, A.
dc.contributor.authorHowes, O.
dc.contributor.authorMurphy, D.
dc.contributor.authorBorg, J.
dc.date.accessioned2018-12-13T09:13:30Z
dc.date.available2018-12-13T09:13:30Z
dc.date.created2018-12-12T02:47:06Z
dc.date.issued2018
dc.identifier.citationHorder, 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.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/72449
dc.identifier.doi10.1126/scitranslmed.aam8434
dc.description.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.

dc.titleGABAA receptor availability is not altered in adults with autism spectrum disorder or in mouse models
dc.typeJournal Article
dcterms.source.volume10
dcterms.source.number461
dcterms.source.issn1946-6234
dcterms.source.titleScience Translational Medicine
curtin.departmentSchool of Occ Therapy, Social Work and Speech Path
curtin.accessStatusFulltext not available


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