Antagonism and neurocomputational mechanisms of cooperation

About This Grant

Problems in cooperating with others define antagonism, a transdiagnostic dimension of psychopathology expressed in personality and externalizing disorders. People high on antagonism are prone to aggressive, callous, and exploitative behaviors that damage relationships and incur substantial costs in the form of productivity loss, substance misuse, and criminality. While clinical theories link antagonism to deficits in social cognition, it is hard to deny that exploiting others requires an understanding of their mind. This apparent contradiction can be resolved by distinguishing between two facets of antagonism: callousness and exploitativeness. Our prior work and preliminary data inform the hypothesis that exploitativeness reflects an enhanced capacity to learn about the mental states and behaviors of others coupled with an increased sensitivity to personal, rather than shared, rewards. In contrast, callousness reflects a broader insensitivity to social feedback. We hypothesize that these dissociable social learning processes are instantiated in canonical circuits that expanded during anthropogenesis to support mentalizing and self-directed thought. These learning signals, which track behaviorally salient features of the social environment, are integrated in the posterior hub of the default network where they drive adaptive cooperation. We will test these hypotheses in two samples elevated on antagonism. At the behavioral level, we will characterize participants using a battery of personality and psychopathology measures, social and reward-based decision-making tasks, and corresponding hierarchically estimated reinforcement learning models (Aim 1). In a model-based fMRI study of our existing longitudinal clinical cohort, we will link model-derived learning signals and facets of antagonism to underlying neural activity during cooperative decision-making (Aim 2). Leveraging the multi-timescale design of our study, we will relate neurocomputational signatures of callousness and exploitativeness to mentalizing abilities, multi- informant reports of momentary interpersonal behavior, and prospective stress generation. The interdisciplinary investigative team assembled for this project has expertise in quantitative models of personality and psychopathology (Allen, Pilkonis), interpersonal theory (Allen, Pilkonis, Hallquist), experimental design (Dombrovski, FeldmanHall), social computational neuroscience (Allen, Dombrovski, Hallquist, FeldmanHall), imaging methods (Hallquist), multi-informant ecological momentary assessment (Pilkonis), and stress generation (Allen, Slavich). In line with the NIMH’s Strategic Objectives, the proposed work will reveal the brain mechanisms underlying critical social processes and characterize neural circuit mechanisms that contribute to human behavior and psychopathology. Our approach bridges modern dimensional models of psychopathology with the RDoC framework, integrating across multiple levels of analysis to elucidate human social processes, and shed light on the ways we perceive and understand others.