Siberian hamsters (Phodopus sungorus) express daily torpor, decreasing body temperature to ~15 °C and providing a significant savings in energy expenditure. Daily torpor in hamsters is cued by winter-like photoperiods, occurring coincident with annual nadir in body fat and chronic leptin concentrations. To better understand the neural mechanisms underlying torpor, Siberian hamsters were perinatally treated with saline or MSG to ablate arcuate nucleus neurons that likely possess leptin receptors. Body temperature was studied telemetrically in cold-acclimated (10 °C) hamsters moved to a winter-like photoperiod (10 h light: 14 h dark) (Exps. 1 & 2) or that remained in a summer-like photoperiod (14 h light: 10 h dark ) (Exp. 3). In Exp. 1, even though other photoperiodic responses persisted, MSG-induced arcuate nucleus ablations prevented the photoperiod-dependent torpor observed in saline-treated Siberian hamsters. MSG-treated hamsters tended to possess greater fat reserves. To determine whether reductions in body fat would increase frequency of photoperiod-induced torpor after MSG-treatment, hamsters underwent 2 weeks of food-restriction (70% of ad lib) in Exp. 2. Although food-restriction did increase the frequency of torpor in both MSG- and saline-treated hamsters, it failed to normalize the proportion of MSG-treated hamsters undergoing torpor. In Exp. 3, postnatal MSG treatments reduced the proportion of hamsters entering 2DG-induced torpor-like hypothermia by ~50% compared to saline-treated hamsters (38 vs. 72%). We conclude that: 1) arcuate nucleus mechanisms mediate photoperiod-induced torpor, 2) food-restriction-induced torpor may also be reduced by MSG treatments, and 3) arcuate nucleus neurons also contribute to 2DG-induced torpor-like hypothermia.