UT Southwestern Medical Center researchers identified a key molecular mechanism that regulates the brain’s ability to mentally compensate for sleep deprivation.

The researchers found that a molecule called an adenosine receptor is necessary for sleep-restricted animals to attain adequate levels of slow-wave activity in the brain once normal sleep resumes through their work with mice. This increase in slow-wave activity during rebound sleep helps restore normal working memory and attention skills to the sleep-deprived.
“Normal society pushes people to burn candles at both ends—going to bed late, getting up early, and somehow performing mentally with lack of adequate sleep,” says senior author Robert Greene, MD, PhD, professor of psychiatry at UT Southwestern, in a press release about the study. “We need to have our adenosine receptors intact to do that.”

Adenosine receptors on nerve cells, including brain cells, act as docking points for the molecule adenosine. Adenosine levels increase in the brain with each hour of waking activity, and in this study “docking” of the molecule with its receptor is shown to help promote the slow-wave activity of sleep.

Additionally, these findings explain the effects of caffeine, which also “docks” to adenosine receptors, preventing the docking of adenosine and keeping the caffeine drinker awake.

“They probably won’t get the regular amount of slow-wave activity or deep sleep as they normally would,” says Greene. “This is not to say that coffee is bad, but drinking it all the time or in the evening could affect your mental performance the next day.”

The study appears in the Journal of Neuroscience.