Odor-evoked activity outside canonical areas of olfactory information transmission is visualized by ODORTRAP and modulated by diet-induced obesity

Abstract

Enhanced excitability of output neurons in the olfactory bulb (OB) has been linked to regulation of energy homeostasis. The mechanism by which the olfactory system can drive metabolic state while processing odor information remains elusive yet must depend upon integration and relay to the rest of the brain. Herein, we screened brain-wide neuronal ensembles that preferentially engaged during odor stimulation (referred to as ODORTRAP) utilizing FOSTRAP activity mapping. Mice were exposed to the odor isopropyl tiglate (IPT), a preferred ligand for the olfactory receptor 160, previously shown to be vulnerable to diet-induced obesity. Odor activation resulted in elevated labelling in the olfactory bulb (ODORTRAP) (p 0.05). In mice that were maintained on moderately high-fat (MHF) diets, we discovered that obesity re-models the activation pattern across the brain. Obese mice exhibited loss of ODORTRAP activity in the ARC (p 0.05). Our study identifies key brain regions linking chemosensation and metabolic state, specifically demonstrating alteration in activity in hypothalamic domains upon obesogenic diet.