A major driver of obesity is the increasing palatability of processed foods. Although reward circuits promote the consumption of palatable food their involvement in obesity remains unclear. The ventral pallidum (VP) is a key hub in the reward system that encodes the hedonic aspects of palatable food consumption and participates in various proposed feeding circuits. However, there is still no evidence for its involvement in developing diet-induced obesity. Here we examine, using male C57bl6/J mice and patch-clamp electrophysiology, how chronic high-fat-high-sugar (HFHS) diet changes the physiology of the VP and whether mice that gain the most weight differ in their VP physiology from others. We found that 10-12 weeks of HFHS diet hyperpolarized and decreased the firing rate of VP neurons without a major change in synaptic inhibitory input. Within the HFHS group, the top 33% weight gainers (WG) had a more hyperpolarized VP with longer latency to fire action potentials upon depolarization compared to bottom 3...