Jacqueline N. Crawley, Ph.D., received a B.A. in Biology from the University of Pennsylvania in 1971, Ph.D. in Zoology from the University of Maryland in 1976, and completed a postdoctoral fellowship in Neuropsychopharmacology at Yale University School of Medicine in 1979. She directs the Laboratory of Behavioral Neuroscience at the National Institute of Mental Health Intramural Research Program in Bethesda. Her research focuses on generating mouse models of neuropsychiatric disorders, to test hypotheses about genetic and neuropharmacological mechanisms, and to evaluate treatment efficacy. She is the author of a widely used book, What's Wrong With My Mouse? Behavioral Phenotyping of Transgenic and Knockout Mice (Wiley, 2000, 2007).

Recent interests in developing mouse models of autism arose from Dr. Crawley's recognition of the remarkably high heritability of autism, the likelihood that strong candidate genes will be discovered, and emerging opportunities for evaluating candidate genes in mice with analogous targeted gene mutations. How do you model the symptoms of autism in mice, to evaluate the consequences of the mutation? Our lab engaged in this challenging problem, to develop appropriate mouse behavioral tasks with face validity for the diagnostic and associated behavioral symptoms of autism. In 2004, our team invented an automated three-chambered social approach task for mice that is employed by many other labs for phenotyping mouse models of autism. Over the past five years, we developed a large set of mouse behavioral tasks relevant to all three diagnostic domains of autism. Currently we phenotype each autism candidate gene mutant line using the automated social approach task, reciprocal social interaction tasks for juveniles and adults, ultrasonic vocalization analyses in pups, juveniles, and adults, social olfactory tests, measures of motor stereotypies, perserveration tasks for repetitive behaviors, and holeboard approaches to evaluating restricted interests in mice. A battery of relevant control parameters are routinely conducted, to assay for physical disabilities that could confound the interpretation of autism-relevant phenotypes. Recent publications include the behavioral phenotypes of oxytocin knockouts, neuroligin-3 knockins, and the BTBR T+tf/J inbred strain. We are now investigating interventions, including behavioral and drug treatments, that may reverse the robust autism-relevant behavioral abnormalities in BTBR T+tf/J, towards developing therapeutics for the core symptoms of autism.