Production Report


The palatability of food is related to food pleasantness (hedonic value) and promotes a transition from ‘‘sampling to savoring’’ that extends consumption behavior (Yeomans, 1998). Hunger increases subjective accounts of palatability in humans (Cabanac, 1971). The increasing prevalence of obesity may also be driven by simple access to cheap and highly palatable food (Johnson and Wardle, 2014). Palatability is a main factor that influences appetite (Sørensen et al., 2003), but little is known about the relationship between the neural circuits through which hunger increases consumption and shifts palatability and the interoceptive sensory neurons. Hunger is not the only factor that regulates ingestion. Thirst increases the consumption of water by nitric oxide synthase 1 (Nos1)- expressing neurons in the suprafornical organ (SFONOS1) that selectively promote water seeking, generate thirst-related brain state changes, and detect physiological dehydration (Allen et al., 2019; Betley et al., 2015; Oka et al., 2015; Zimmerman et al., 2016). Thirst and hunger circuits related to SFONOS1 neurons and AGRP neurons are mainly considered find out here as discrete interoceptive pathways for individual physiological states. Less attention has been given to the behavioral mechanisms that are shared between these distinct physiological states and the possible convergence of thirst and hunger circuits. To investigate this gap in the literature, the separately localized and molecularly defined SFONOS1 and AGRP neurons were used as entry points to evaluate the convergence of thirst and hunger circuits. Glutamatergic neurons in the anterior peri-locus coeruleus (periLC) were identified as a polysynaptic convergence region in thirst and hunger processes. Causal perturbations and circuit dynamics demonstrate that periLC neurons regulate eating and drinking by controlling palatability during the consummatory behavior phase.

2020-12-01 / Posted in