Journal
SCIENCE TRANSLATIONAL MEDICINE
Volume 10, Issue 461, Pages -Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/scitranslmed.aam8434
Keywords
-
Categories
Funding
- EU AIMS
- AIMS-2-TRIALS
- IMI Joint Undertaking (JU) [115300]
- European Union's Seventh Framework Programme (FP7/2007-2013)
- European Federation of Pharmaceutical Industries and Associations (EFPIA)
- Autism Speaks
- IMI 2 JU [777394]
- European Union's Horizon 2020 research and innovation programme
- EFPIA
- Autistica
- Simons Foundation Autism Research Initiative
- Wellcome Trust [091300/Z/10/Z]
- Biomedical Research Centre (BRC) at King's College London
- Swedish Research Council [523-2013-2982]
- Mortimer D. Sackler Foundation
- National Institute for Health Research BRC at South London and Maudsley NHS (National Health Service) Foundation Trust and King's College London
- Swedish Brain Foundation
- Stockholm Brain Institute
- Thuring Foundation
- Medical Research Council, UK [MC-A656-5QD30]
- MRC [MR/K022733/1, MC_U120097115, MR/N026063/1, G1002226] Funding Source: UKRI
- Wellcome Trust [091300/Z/10/Z] Funding Source: Wellcome Trust
Ask authors/readers for more resources
Preliminary studies have suggested that gamma-aminobutyric acid type A (GABA(A)) receptors, and potentially the GABA(A) alpha 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 GABA(A) and GABA(A) alpha 5 receptor availability in two positron emission tomography imaging studies. We used the tracer [C-11]flumazenil in 15 adults with ASD and in 15 control individuals without ASD and the tracer [C-11]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 GABA(A) receptor or GABA(A) alpha 5 subunit availability in any brain region of adults with ASD compared to those without ASD. There were no differences in GABA(A) receptor or GABA(A) alpha 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 GABA(A) receptor availability may be normal in adults with ASD, although GABA signaling may be functionally impaired.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available