Mechanisms underlying social reward deficits in autism
Autism is a highly prevalent neurodevelopmental disease, affecting approximately 1 in 150 children; yet, at this time there is no cure. The disorder is characterized by core deficits in social function, including a profound lack of interest in others. Perhaps the most straightforward hypothesis about how this "autistic aloneness" develops, is that for people with autism, social interactions are simply not rewarding, or, are in some way abnormally rewarding. Interestingly, evidence from human imaging suggests that the brain regions that enable these functions may converge at the mesocorticolimbic reward circuit. My previous work as a postdoctoral fellow has implicated the nucleus accumbens, a key node of this reward circuit, in encoding social reward; however, it remains to be seen whether these mechanisms are disrupted in mouse models of autism. As a new investigator seeking my first independent funding, I propose here to investigate the synaptic and circuit mechanisms underlying social reward deficits in autism. Guided by these mechanistic insights, our goal will be to develop novel therapeutic interventions for autism, which target the relevant circuit using cutting-edge, light-activated "optogenetic" technologies.