Despite a broad continuum of phenotypic variation in behavior, individuals with autism spectrum disorders (ASD) share core deficits in social interaction. Here we propose that social dysfunction in ASD results, in part, from impairments in deriving vicarious reinforcement from others. Observing what happens to others powerfully shapes normal human learning and behavior. Such other-regarding outcomes can drive observational learning, and motivate behaviors such as cooperation, as well as envy. Empathic responses associated with vicarious reward appear early in ontogeny, and their impairment in neuropsychiatric disorders like ASD can have devastating consequences. Understanding and treating social dysfunction in ASD will be advanced by discovering and manipulating the neural mechanisms that derive vicarious reward and punishment from what happens to others. Although brain-imaging studies have revealed some of the neural circuitry mediating social interactions, the neuronal mechanisms underlying vicarious reward remain unknown. We will use our new behavioral model of vicarious reward to determine the underlying neuronal mechanisms, delineate the impacts of network dysfunction due to reversible inactivation of ACC or OFC on vicarious reward and other-regarding behavior, and define the effects of oxytocin (OT), a potential therapeutic intervention for ASD, on behavior and neural function.

Public Health Relevance

Despite a broad continuum of phenotypic variation in behavior, individuals with autism spectrum disorders (ASD) share core deficits in social interaction. Here we propose that social dysfunction in ASD results, in part, from problems in deriving vicarious reward from others. We will use our new animal model of vicarious reward to discover how the brain signals vicarious reward, discover the impact of brain dysfunction on vicarious reward, and test how oxytocin, a potential therapy for ASD, might improve vicarious reward and brain function.

Agency
National Institute of Health (NIH)
Institute
National Institute of Mental Health (NIMH)
Type
Research Project (R01)
Project #
5R01MH095894-03
Application #
8598108
Study Section
Biobehavioral Regulation, Learning and Ethology Study Section (BRLE)
Program Officer
Rossi, Andrew
Project Start
2012-02-21
Project End
2016-11-30
Budget Start
2013-12-01
Budget End
2014-11-30
Support Year
3
Fiscal Year
2014
Total Cost
$278,785
Indirect Cost
$98,785
Name
Duke University
Department
Other Basic Sciences
Type
Schools of Arts and Sciences
DUNS #
044387793
City
Durham
State
NC
Country
United States
Zip Code
27705
Platt, Michael L; Seyfarth, Robert M; Cheney, Dorothy L (2016) Adaptations for social cognition in the primate brain. Philos Trans R Soc Lond B Biol Sci 371:20150096
Drucker, Caroline B; Carlson, Monica L; Toda, Koji et al. (2015) Non-invasive primate head restraint using thermoplastic masks. J Neurosci Methods 253:90-100
Chang, Steve W C; Fagan, Nicholas A; Toda, Koji et al. (2015) Neural mechanisms of social decision-making in the primate amygdala. Proc Natl Acad Sci U S A 112:16012-7
Ebitz, R Becket; Platt, Michael L (2015) Neuronal activity in primate dorsal anterior cingulate cortex signals task conflict and predicts adjustments in pupil-linked arousal. Neuron 85:628-40
Chang, Steve W C; Platt, Michael L (2014) Oxytocin and social cognition in rhesus macaques: implications for understanding and treating human psychopathology. Brain Res 1580:57-68
Utevsky, Amanda V; Platt, Michael L (2014) Status and the brain. PLoS Biol 12:e1001941
Brent, Lauren J N; Chang, Steve W C; Gariepy, Jean-Francois et al. (2014) The neuroethology of friendship. Ann N Y Acad Sci 1316:1-17
Pearson, John M; Watson, Karli K; Platt, Michael L (2014) Decision making: the neuroethological turn. Neuron 82:950-65
Ebitz, R Becket; Pearson, John M; Platt, Michael L (2014) Pupil size and social vigilance in rhesus macaques. Front Neurosci 8:100
Roy, Arani; Shepherd, Stephen V; Platt, Michael L (2014) Reversible inactivation of pSTS suppresses social gaze following in the macaque (Macaca mulatta). Soc Cogn Affect Neurosci 9:209-17

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