Autism is characterized by profound social impairments. There is little understanding of the origin of these social deficits, and efficient diagnosis and therapeutic options are lacking. Molecular genetic approaches allow for the discovery of specific neural circuits involved in social behavior, facilitating the development of diagnostics and therapeutic approaches specific to social deficits.
Catherine Dulac and her team at Harvard University have carried out multifaceted investigations of neural circuits underlying mouse social recognition using advanced molecular, genetic and behavioral approaches. They aim to investigate the function of the evolutionarily conserved neuropeptide oxytocin and its receptor in facilitating sensory processing of social cues, using the mouse as a model system.
Oxytocin and its receptor act on the central nervous system to regulate social behaviors, and have been consistently implicated in the pathogenesis of autism. Mice deficient in oxytocin have profound social behavior deficits, including failure to distinguish between familiar and novel mice, deficits in maternal behavior, abnormal inter-male aggression and increased fear and anxiety. Mice lacking oxytocin show different neuronal activation patterns in response to social interactions than controls do. These deficits are reminiscent of findings in which individuals with autism display impairments in facial memory, have decreased activation of the amygdala and cortical areas for face recognition when viewing images of faces, and increased activation in nonsocial cortical regions when viewing images of faces.
Dulac and her colleagues aim to investigate the role of oxytocin in mediating appropriate behavioral responses to social information, providing clues for the social interaction defects of autism. As a pilot study, they hope to investigate whether oxytocin is required for mice to distinguish between specific social cues. They also aim to analyze behavioral phenotypes relevant to autism and explore the potential neuronal changes leading to the observed social interaction defects.