Strategies for developing and studying animal models of autism have focused on social and communication function using a different battery of tests. In mouse models, the olfactory (smell) system serves as a basis for investigating social interaction, thus knowledge of the proper functioning of this system is necessary to determine the mechanisms by which these behaviors are disrupted. Dr. Gelperin and colleagues will be studying the olfactory system in a mouse model which is genetically engineered to be deficient in receptors for a critical social communication peptide (pituitary adenylate cyclase activating peptide or PAC). Specifically, the processing of social signals for mating and social behavior will be measured together with neuronal activity in the olfactory centers of the mouse brain during these tasks. By investigating the cellular and physiological responses of olfactory neurons during tasks which involve social signals, the neural basis of social reciprocity will be better understood. Significance: The proposed work will test a specific hypothesis about the underlying neurological mechanism of impaired social reciprocity in PAC1-/- mice. If the proposed work indicates that social reciprocity disruption arises from abnormal timing relations of network activity in the olfactory system, it might be possible to extrapolate to human and provide neurobiological insight into one of the core deficits of autism.