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Slow-wave activity during sleep affected by quality, intensity of wakefulness
February 01, 2007WESTCHESTER, Ill. — A study published in the February 1st issue of the journal SLEEP provides a first direct demonstration that the "quality" and "intensity" of wakefulness can affect slow-wave activity (SWA) during subsequent sleep.
According to Chiara Cirelli, MD, PhD, of the University of Wisconsin-Madison, one of the authors of the study, the importance and novelty of the paper lies in the demonstration that the crucial factor linking physiological waking activity to sleep SWA is synaptic plasticity, notably synaptic potentiation, mediated by brain-derived neurotrophic factor (BDNF) signaling.
"Namely, the study shows that wakefulness associated with exposure to an enriched environment and with high levels of exploratory activity, a condition well known to trigger plastic changes in the brain, leads to increased BNDF expression and increased sleep pressure as compared to wakefulness with low exploratory activity," said Cirelli. "More stringently, the study finds that the amount of exploratory behavior during wakefulness can predict the extent to which BDNF is induced in the cerebral cortex, as well as the extent of the SWA response during subsequent sleep."
Cirelli notes that SWA has been validated as the best current marker of sleep pressure and sleep intensity by more than 30 years of research, and yet there is very poor understanding of the crucial factors that determine how and why sleep pressure increases during wakefulness and decreases during sleep.
"This paper offers a first hint of what may be at least one of the crucial factors linking the 'quality' of wakefulness to the intensity of sleep," added Cirelli.
The study is also novel in the approach used to prove this point, a combination of electroencephalographic, behavioral and molecular methods, said Cirelli, adding that the results of the study strongly support the hypothesis that synaptic plasticity during wakefulness is linked to sleep homeostasis. These findings complement other data recently published by Cirelli and her colleagues showing that the cortical areas more actively involved in the learning of a motor task during waking show the largest increase in SWA during subsequent sleep.
American Academy of Sleep Medicine
Cirelli notes that SWA has been validated as the best current marker of sleep pressure and sleep intensity by more than 30 years of research, and yet there is very poor understanding of the crucial factors that determine how and why sleep pressure increases during wakefulness and decreases during sleep.
"This paper offers a first hint of what may be at least one of the crucial factors linking the 'quality' of wakefulness to the intensity of sleep," added Cirelli.
The study is also novel in the approach used to prove this point, a combination of electroencephalographic, behavioral and molecular methods, said Cirelli, adding that the results of the study strongly support the hypothesis that synaptic plasticity during wakefulness is linked to sleep homeostasis. These findings complement other data recently published by Cirelli and her colleagues showing that the cortical areas more actively involved in the learning of a motor task during waking show the largest increase in SWA during subsequent sleep.
American Academy of Sleep Medicine
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