Atypical sensory processing is a proposed etiological factor underlying the development of behavioral deficits in autism spectrum disorder (ASD). In particular, hypo-responsiveness to sensory social stimuli reduces social orienting, thus limiting the number of opportunities in which social learning can occur. Indeed, poorer social communication skills in individuals with ASD are associated with hypo-responsiveness to multiple sensory modalities.
The oxytocin (OT) system is critically involved in the regulation of a wide array of species-typical social behaviors, including social orienting. Interestingly, during early periods of development, both general sensory deprivation and an impoverished social world can dramatically attenuate signaling within the OT system. Moreover, reduced OT-signaling is associated with abnormal development of all primary sensory cortical regions1. Given the importance of OT in the proper display of social behavior, as well as in the development of the sensory cortices, it is possible that aberrant OT signaling may contribute to characteristic symptoms seen in ASD.
Garret Stuber and his colleagues at the University of North Carolina at Chapel Hill propose to utilize novel in vivo imaging methods to directly measure the activity of OT neurons in typically developing mice and in SHANK3 knockout mice, which have previously been shown to have social deficits2. Additionally, the team plans to examine how the OT system regulates somatosensory processing of social cues. Examination of these interacting systems will greatly increase our understanding of the behavioral context in which OT functions and how the OT system contributes to the recognition of a stimulus as a salient social signal, thus furthering our understanding of mechanisms potentially underlying social communication deficits in ASD.