Torpor, a state characterized by a well-orchestrated reduction of metabolic rate and body temperature (T_b) is employed for energetic savings by organisms throughout the animal kingdom. The nucleotide AMP has recently been purported to be a primary regulator of torpor in mice, as circulating AMP is elevated in the fasted state and administration of AMP causes severe hypothermia. However, we have found that the characteristics and parameters of the hypothermia induced by AMP were dissimilar to those of fasting-induced torpor bouts in mice. While administration of AMP induced hypothermia (min. T_b = 25.2 ± 0.6 °C), similar to the depth of fasting-induced torpor (24.9 ± 1.5 °C), ), ADP and ATP were equally effective in lowering T_b (min.T_b: 24.8 ± 0.9 °C and 24.0 ± 0.5 °C, respectively). The maximum rate of T_b fall into hypothermia was significantly faster with injection of adenine nucleotides (AMP- 0.24 ± 0.03; ADP- 0.24 ± 0.02; ATP- 0.25 ± 0.03 °C/min) than during fasting-induced torpor (0.13 ± 0.02 °C/min). Heart rate decreased from 755 ± 15 to 268 ± 17 bpm within one minute of AMP administration, much different from that observed during torpor (646 ± 21 to 294 ± 19 bpm over 35 minutes). Finally, the hypothermic effect of AMP was blunted with pre-administration of an adenosine receptor blocker, suggesting that AMP action on T_b is mediated via the adenosine receptor. These data suggest that injection of adenine nucleotides into mice induces a reversible hypothermic state that is unrelated to fasting-induced torpor.