A hallmark of autism spectrum disorders is impaired social interactions. Several studies show that neural systems that support social interaction overlap with those responsible for the perception of reward. The poor responsiveness to social stimuli seen in individuals with autism could therefore reflect a failure to attribute reward value to social interactions.
Christian Luscher and his colleagues at the University of Geneva aim to test this hypothesis by investigating whether social reward, like addictive drug use, elicits changes in the ventral tegmental area (VTA), a region of the midbrain that contains dopamine neurons and has been implicated in reward circuitry. They plan to focus on changes at the synapses — points of contact between neurons — known as reward-evoked plasticity. The group plans to combine electrophysiological techniques with behavioral observations in mice to explore the reward system. Luscher’s group also plans to study the postnatal development of excitatory nerve transmission to better understand the physiology that underlies this plasticity. One protein of particular interest in this context is SHANK3. Mutations in the SHANK3 gene have been associated with specific forms of autism, and preliminary data show that it is a key player in the development of excitatory activity of dopamine neurons in the VTA.
A better understanding of the neural mechanisms of reward-driven learning, and how these mechanisms contribute to social interactions, may provide insight into the neural basis of autism spectrum disorders and open doors to new treatments.
