Siberian hamsters (Phodopus sungorus) undergo bouts of daily torpor during which body temperature decreases by as much as 20 degrees C and provides a significant savings in energy expenditure. Natural torpor in this species is normally triggered by winter-like photoperiods and low ambient temperatures. Intracerebroventricular injection of neuropeptide Y (NPY) reliably induces torpor-like hypothermia that resembles natural torpor. NPY-induced torpor-like hypothermia is also produced by intracerebroventricular injections of an NPY Y1 receptor agonist but not by injections of an NPY Y5 receptor agonist. In this research, groups of cold-acclimated Siberian hamsters were either co-injected with a Y1 receptor antagonist (1229U91) and NPY or were co-injected with a Y5 receptor antagonist (CGP71683) and NPY in counterbalanced designs. Paired saline + NPY induced torpor-like hypothermia in 92% of the hamsters, whereas co-injection of Y1 antagonist + NPY induced torpor-like hypothermia in 4% of the hamsters. In contrast, paired injections of saline + NPY and Y5 antagonist + NPY induced torpor-like hypothermia in 100% and 91% of the hamsters, respectively. Although Y5 antagonist treatment alone had no effect on body temperature, Y1 antagonist injections produced hyperthermia compared to controls. Both Y1 antagonist and Y5 antagonist injections significantly reduced food ingestion 24 hours after treatment. We conclude that activation of NPY 1 receptors are both sufficient and necessary for NPY-induced torpor-like hypothermia.