Sleep homeostatis, therefore, does not play a significant role in the timing or the onset of the arousal episodes. Since sleep debt does not appear to be the trigger that initiates euthermy in hibernating animals, a different internal cue must control the onset of euthermy. Research focuses now on the connection between euthermy and synaptogenesis. Low hibernation temperatures are known to decrease electrical brain activity. Adenosine is one of the chemicals that may act as a trigger that initiates euthermy and, simultaneously, act as an energy conservation measure by inducing sleep during arousal.
Adenosine acts as both an inhibitor of neuronal activity as well as a sleep-inducer.
These two functions, although quite distinctive, correlate well with the proposed theories of euthermy. Adenosine controls neurons whose discharge activity plays a large role in the elevation of EEG readings by inhibiting postsynaptically the hyperpolarization-activated current of the neurons. Adenosine levels decrease in the brain as neuronal activity increases, and recovery sleep replenishes both the sleep deficit and the temperature-hindered neuronal activity. EEG readings and adenosine levels are directly proportional to each other. Adenosine, or perhaps a similar chemical, could reach a threshold corresponding to a low level of neuronal discharge and induce euthermy in an organism.