DALLAS Feb. 24, 2009 Sleep experts know that the mental clarity lost because of a few sleepless nights can often be restored with a good night's rest. Now, UT Southwestern Medical Center researchers have identified a key molecular mechanism that regulates the brain's ability to mentally compensate for sleep deprivation.
Working with mice, they 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. It is this increase in slow-wave activity, or SWA, during rebound sleep that helps restore normal working memory and attention skills to the sleep-deprived, the scientists report in the Feb. 4 issue of the Journal of Neuroscience.
"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," said senior author Dr. Robert Greene, professor of psychiatry at UT Southwestern. "We need to have our adenosine receptors intact to do that."
Adenosine receptors on nerve cells, including brain cells, are akin to docking points for the molecule adenosine. Adenosine levels increase in the brain with each hour of waking activity, and "docking" of the molecule with its receptor is shown in this study to help promote the slow-wave activity of sleep. Scientists have known that recovery from sleep deprivation involves not only an increase in sleep time, or rebound sleep, but also an elevation in this slow-wave activity.
To investigate how adenosine receptors and SWA might be linked, Dr. Greene and his team engineered mice that lacked a receptor to pair up with adenosine.
Sleep-restricted mice were kept awake by being placed on a moving treadmill. Researchers then electronically monitored sleep and waking activity of both normal and genetically engineered mice, including monitoring electronically the brain waves
|Contact: LaKisha Ladson|
UT Southwestern Medical Center