Controlling hibernation

Tulasi Jinka, Øivind Tøien, and Kelly L. Drew of the University of Alaska Fairbanks were able to induce torpor in arctic ground squirrels, but only during their normal hibernation cycles.  They were also able to bring animals out of hibernation at will.

Hibernation involves lowering the metabolism to a nearly deathlike state, a condition known as torpor.  A hibernating animal might have a core body temperature barely above freezing, and use as little as one percent of the amount of oxygen it would require while active. 

One of the molecules known to regulate torpor is adenosine.  When this nucleotide binds to specific receptors, it inhibits the central nervous system.  In humans, this results in the drowsy feeling that tells us it’s time for bed.  In arctic ground squirrels, the binding of adenosine to its receptor induces hibernation.  Receptors like the one to which adenosine attaches can be bound by other molecules as well.  Agonists and antagonists also park at the receptor’s binding site, the former inducing the normal activity and the latter blocking it.  Caffeine is an example of an adenosine antagonist.

The researchers gave six ground squirrels adenosine agonists and antagonists at three different stages of their yearly cycles:  during the summer, at the very start of the hibernation period, and midway through hibernation.  During the last time period, squirrels were first woken up so that they could be put back to sleep.  The agonists induced torpor during the normal hibernation periods (and did so especially well in the squirrels awoken while already hibernating) but not all during the summer.  In contrast, an adenosine antagonist was able to reverse spontaneous entry into torpor. 

Besides generating a pack of extremely grouchy ground squirrels, this research might one day lead to more precise control of hibernation.  If so, perhaps humans, who after all also have adenosine receptors, could be brought into a state of torpor for medical or intergalactic travel purposes.