Exogenous and evoked oxytocin restores social behavior in the Cntnap2 mouse model of autism

Author:

Peñagarikano Olga12,Lázaro María T.1,Lu Xiao-Hong3,Gordon Aaron4,Dong Hongmei1,Lam Hoa A.5,Peles Elior4,Maidment Nigel T.5,Murphy Niall P.5,Yang X. William3,Golshani Peyman167,Geschwind Daniel H.123

Affiliation:

1. Program in Neurogenetics, Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, USA.

2. Center for Autism Research and Treatment and Center for Neurobehavioral Genetics, Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA 90095, USA.

3. Center for Neurobehavioral Genetics, Department of Psychiatry and Biobehavioral Sciences, University of California, Los Angeles, Los Angeles, CA 90095, USA.

4. Department of Molecular Cell Biology, Weizmann Institute of Science, Rehovot 76100, Israel.

5. Department of Psychiatry and Biobehavioral Sciences, Jane and Terry Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles, Los Angeles, CA 90095, USA.

6. Integrative Center for Learning and Memory, University of California, Los Angeles, Los Angeles, CA 90095, USA.

7. West Los Angeles VA Medical Center, Los Angeles, CA 90073, USA.

Abstract

Mice carrying a genetic mutation that causes autistic symptoms show improved sociability after being treated with oxytocin, a hormone promoting mothering and trust.

Funder

NIH

National Institute of Mental Health (NIMH)

NIH/National Institute of Neurological Disorders and Stroke (NINDS)

Autism Speaks

Simons Foundation Autism Research Initiative

McKnight Foundation

NIH Autism Centers of Excellence (ACE)

Network

UCLA Center for Autism Research and Treatment (CART) Pilot

Publisher

American Association for the Advancement of Science (AAAS)

Subject

General Medicine

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