Food consummatory behavior is a complex process that serves to maintain physiological homeostasis while simultaneously encoding the hedonic properties of food [1]. Hedonic foods (i.e., foods high in sugar and fat) are more reinforcing than low-calorie foods and robustly activate brain regions driving motivation, which promotes overconsumption regardless of homeostatic state. This hedonic “override” is thought to contribute to weight gain and obesity. As highly palatable foods continue to become more accessible and rates of the metabolic disease continue to increase, it is evident that there is a crucial need to enhance our understanding of the neural circuits that integrate homeostatic and hedonic pathways to identify novel therapeutic strategies to restore balanced consummatory behaviors.

The nucleus accumbens (NAc) is a brain region involved in motivation and food consumption [2]. In addition, a role for accumbal glutamate in consummatory behavior has been described where intra-NAc administration of AMPA receptor antagonists promotes the intake of food [3]. Although the NAc receives input from the midbrain, cortical, and thalamic structures, much remains to be learned about afferents from structures involved in maintaining homeostasis of consummatory behavior, such as the hypothalamus. Direct neuronal projections from the paraventricular nucleus of the hypothalamus (PVN) to the nucleus accumbens were identified in the context of social reinforcement [4]. In these studies, the PVN was shown to project directly to the NAc to regulate oxytocin and serotonin release and promote the reinforcement of social interactions in mice. However, a role for the PVN → NAc pathway in regulating food intake remained unstudied.

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