Categorically distinct basic drives (for example, for social versus feeding behaviour1,2,3) can exert potent influences on each other; such interactions are likely to have important adaptive consequences (such as appropriate regulation of feeding in the context of social hierarchies) and can become maladaptive (such as in clinical settings involving anorexia). It is known that neural systems regulating natural and adaptive caloric intake, and those regulating social behaviours, involve related circuitry4,5,6,7, but the causal circuit mechanisms of these drive adjudications are not clear. Here we investigate the causal role in behaviour of cellular-resolution experience-specific neuronal populations in the orbitofrontal cortex, a major reward-processing hub that contains diverse activity-specific neuronal populations that respond differentially to various aspects of caloric intake8,9,10,11,12,13 and social stimuli14,15. We coupled genetically encoded activity imaging with the development and application of methods for optogenetic control of multiple individually defined cells, to both optically monitor and manipulate the activity of many orbitofrontal cortex neurons at the single-cell level in real time during rewarding experiences (caloric consumption and social interaction). We identified distinct populations within the orbitofrontal cortex that selectively responded to either caloric rewards or social stimuli, and found that activity of individually specified naturally feeding-responsive neurons was causally linked to increased feeding behaviour; this effect was selective as, by contrast, single-cell resolution activation of naturally social-responsive neurons inhibited feeding, and activation of neurons responsive to neither feeding nor social stimuli did not alter feeding behaviour. These results reveal the presence of potent cellular-level subnetworks within the orbitofrontal cortex that can be precisely engaged to bidirectionally control feeding behaviours subject to, for example, social influences.
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The data that support the finding of this study are available upon request from the corresponding author.
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We thank members of the Deisseroth laboratory for input and discussions, and particularly A. Crow for assistance with microscopy-related tasks. K.D. is supported by the Defense Advanced Research Projects Agency Neuro-FAST program, National Institute of Mental Health, National Institute on Drug Abuse, National Science Foundation, the Simons Foundation, the Tarlton Foundation, the Wiegers Family Fund, the Nancy and James Grosfeld Foundation, the H.L. Snyder Medical Foundation, and the Samuel and Betsy Reeves Fund. This work was also supported by HHWF (J.H.J.), NIDA (C.K.K.), Simons LSRF fellowship (J.H.M.), NSF GRFP (M.R.) and NIDDK (L.Y.).
Nature thanks M. Krashes and the other anonymous reviewer(s) for their contribution to the peer review of this work.