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Steven J Swoap1, Meaghan Rathvon, Margaret Gutilla

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Area of Science:

  • Physiology
  • Metabolic Regulation
  • Animal Models

Background:

  • Torpor is a key energy-saving state involving reduced metabolic rate and body temperature (Tb).
  • Adenosine monophosphate (AMP) has been proposed as a regulator of torpor, with elevated levels in fasted mice and induction of hypothermia upon administration.
  • Previous studies suggested AMP's role in regulating torpor, prompting further investigation into its effects and comparison with natural torpor states.

Purpose of the Study:

  • To investigate the characteristics of AMP-induced hypothermia in mice.
  • To compare AMP-induced hypothermia with fasting-induced torpor in mice.
  • To elucidate the mechanism underlying AMP-induced hypothermia.

Main Methods:

  • Administration of adenine nucleotides (AMP, ADP, ATP) to mice to induce hypothermia.
  • Measurement of body temperature (Tb) and heart rate.
  • Comparison of hypothermia parameters (depth, rate of Tb fall, heart rate changes) with fasting-induced torpor.
  • Assessment of the role of adenosine receptors using an adenosine receptor blocker.

Main Results:

  • AMP, ADP, and ATP induced rapid hypothermia with a significantly faster rate of Tb fall compared to fasting-induced torpor.
  • Heart rate reduction was immediate and rapid following nucleotide administration, unlike the gradual decrease during torpor.
  • The hypothermic effect of AMP was attenuated by an adenosine receptor blocker, indicating mediation via adenosine receptors.
  • Nucleotide-induced hypothermia exhibited distinct characteristics from natural torpor, despite similar Tb reduction depths.

Conclusions:

  • Injection of adenine nucleotides (AMP, ADP, ATP) induces a rapid, reversible hypothermic state in mice.
  • This nucleotide-induced hypothermia is mechanistically distinct from fasting-induced torpor.
  • The effects of adenine nucleotides on Tb are mediated through adenosine receptors.