Individuals with Autism Spectrum Disorder Show Normal Responses to a Fear Potential Startle Paradigm Raphael Bernier, 1,2 Geraldine Dawson, 1 Heracles Panagiotides, 1 and Sara Webb 1 The present study utilized a fear potentiated startle paradigm to examine amygdala function in individuals with autism spectrum disorder. Two competing hypotheses regarding amygdala dysfunction in autism have been proposed: (1) The amygdala is under-responsive, in which case it would be predicted that, in a fear potentiated startle experiment, individuals with autism would exhibit decreased fear conditioning and/or potentiation, and (2) The amygdala is over responsive, in which case an exaggerated potentiation of the startle response would be predicted. Fourteen adolescents and adults diagnosed with autism spectrum disorder and 14 age, gender, IQ, and anxiety level-matched typical adolescents and adults participated. Both participants with autism and typical participants potentiated the startle response following fear conditioning and no group differences in the latency or amplitude of the potentiated startle response were found. These results suggest that this aspect of amygdala function, namely fear conditioning and potentiation of the startle response, is intact in individuals with autism. KEY WORDS: Autism spectrum disorders; amygdala; fear conditioning; potentiated startle. INTRODUCTION Autism is a neurobiological disorder character- ized by impairments in the domains of social inter- action, language and communication, and restricted or repetitive interests and behaviors. Profound impairments in social behavior are believed to be core to the syndrome. While many brain structures and pathways have been suggested to play a role in the disorder, the neurological basis of the disorder is not well understood. A better understanding of the neurobiology of autism would allow for a deeper understanding of the cause of this disorder and more accurate diagnostic measures. Researchers have proposed that amygdala dys- function is a core feature of autism (Baron-Cohen et al., 2000; Schultz et al., 2000). This is based, in part, on autopsy, animal lesion studies, and func- tional imaging studies that have implicated the amygdala in autism and social behavior. In 1970, Kling and colleagues (Kling et al., 1970) studied vervets with amygdala lesions in the wild. The lesioned vervets were unresponsive to their group, failed to display appropriate social signals, withdrew from social interaction and were frequently killed by other members of the group. Amygdala lesioned monkeys fail to initiate social interaction or respond to other monkey’s gestures (Kling & Brothers, 1992), display flat vocalizations that lack affect (Newman & Bachevalier, 1997), and demonstrate reduced mater- nal behaviors, such as suckling, cuddling, and protecting their offspring (Bucher et al., 1970). Such 1 Center on Human Development and Disability, University of Washington, Seattle, WA 98195, USA. 2 Correspondence should be addressed to: Rapheal Berinier, Center on Human Development and Disability, University of Washington, Box 357920, Seattle, WA 98195, USA; Tel.: +1- 206-543-1051; Fax: +1-206-543-5771; e-mail: rab2@u.washing ton.edu. 575 0162-3257/05/1000-0575/0 Ó 2005 Springer ScienceþBusiness Media, Inc. Journal of Autism and Developmental Disorders, Vol. 35, No. 5, October 2005 (Ó 2005) DOI: 10.1007/s10803-005-0002-0