Autism is a neurodevelopmental disorder that affects approximately 1% of the U.S. population. The causes of autism spectrum disorders are under intense investigation, with strong evidence for genetic substrates. Lifetime costs of caring for autistic individuals are high, both in terms of a) quality of life for the affected individuals and their families;b) financial expenses to the families, educational systems, and health care agencies. Discovery of multiple gene mutations, copy number variants, and epigenetic factors in people with autism has spurred the development of mouse models with homologous mutations. Genetic manipulations in mice offer an optimized experimental strategy to understand the consequences of candidate gene mutations. Effective treatments for the core symptoms of autism are currently limited to early behavioral interventions. Discovery of effective pharmacological treatments requires a greater understanding of the risk genes, biological mechanisms, and environmental factors that contribute to the etiology of autism. Animal models with robust phenotypes relevant to the diagnostic symptoms of autism offer an optimized experimental strategy to test the efficacy and safety of proposed treatments. Our Laboratory of Behavioral Neuroscience (LBN) is an international leader in behavioral assays for transgenic and knockout mice with mutations in genes expressed in brain pathways involved in neuropsychiatric disorders. We collaborate with a large number of molecular genetics laboratories that contribute mutant lines of mice with mutations in risk genes for autism to our research program. For FY12 we concentrated on winding down the activities of the laboratory in preparation for the departure of its PI to a new position at another academic institution.

Project Start
Project End
Budget Start
Budget End
Support Year
Fiscal Year
Total Cost
Indirect Cost
U.S. National Institute of Mental Health
Zip Code
Silverman, J L; Oliver, C F; Karras, M N et al. (2013) AMPAKINE enhancement of social interaction in the BTBR mouse model of autism. Neuropharmacology 64:268-82
Wöhr, Markus; Silverman, Jill L; Scattoni, Maria L et al. (2013) Developmental delays and reduced pup ultrasonic vocalizations but normal sociability in mice lacking the postsynaptic cell adhesion protein neuroligin2. Behav Brain Res 251:50-64
Silverman, Jill L; Babineau, Brooke A; Oliver, Chicora F et al. (2013) Influence of stimulant-induced hyperactivity on social approach in the BTBR mouse model of autism. Neuropharmacology 68:210-22
Brielmaier, Jennifer; Matteson, Paul G; Silverman, Jill L et al. (2012) Autism-relevant social abnormalities and cognitive deficits in engrailed-2 knockout mice. PLoS One 7:e40914
Yang, Mu; Bozdagi, Ozlem; Scattoni, Maria Luisa et al. (2012) Reduced excitatory neurotransmission and mild autism-relevant phenotypes in adolescent Shank3 null mutant mice. J Neurosci 32:6525-41
Tsai, Peter T; Hull, Court; Chu, YunXiang et al. (2012) Autistic-like behaviour and cerebellar dysfunction in Purkinje cell Tsc1 mutant mice. Nature 488:647-51
Silverman, Jill L; Smith, Daniel G; Rizzo, Stacey J Sukoff et al. (2012) Negative allosteric modulation of the mGluR5 receptor reduces repetitive behaviors and rescues social deficits in mouse models of autism. Sci Transl Med 4:131ra51
Yang, Mu; Abrams, Danielle N; Zhang, James Y et al. (2012) Low sociability in BTBR T+tf/J mice is independent of partner strain. Physiol Behav 107:649-62
Ey, E; Yang, M; Katz, A M et al. (2012) Absence of deficits in social behaviors and ultrasonic vocalizations in later generations of mice lacking neuroligin4. Genes Brain Behav 11:928-941
Babineau, Brooke A; Yang, Mu; Crawley, Jacqueline N (2012) Mainstreaming mice. Neuropsychopharmacology 37:300-1

Showing the most recent 10 out of 52 publications