Vyazovskiy VV, Olcese U, Hanlon EC, Nir Y, Cirelli C, Tononi G.
Local sleep in awake rats.
Nature. 2011 Apr 28;472(7344):443-7.
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As to the study by Vyazovskiy et al., this is a really elegant demonstration
that full-blown, slow-wave sleep, as indicated by highly synchronized “global”
EEG slow-wave activity and associated neuronal off and on states, develops
from awake periods. They show that, in awake periods, slow-wave activity and associated neuronal on and off periods can also occur, but in waking, these events occur locally in restricted neuron circuits and are not synchronized across wider cortical networks. In fact, with increasing time spent awake, and increasing sleep propensity, such local off states increase in frequency and also occur more often in synchrony with off states in other cortical areas.
These findings very much support the concept originally proposed by Alexander Borbely from the University of Zurich, Switzerland, of a homeostatic sleep regulation that even holds at the level of local cortical neuron populations. It suggests that cortical networks and associated functions that are more or less intensively used during waking develop a kind of “neuronal fatigue” that requires sleep-like off periods to recover, although it is not directly shown in this study that the occurrence of off periods indeed increases during waking as a consequence of prior use of respective neuronal networks. To me, a further intriguing finding of the study is that only local off periods in waking, but not local off periods in sleep, appear to be associated by a transient increase in excitation in neighboring neuron populations. This could hint at a mechanism compensating for the loss of function during off periods which operates locally and is active only during wakefulness. Obviously, there is a point at which the brain switches from waking to sleep, not anymore trying to compensate for such off periods. Overall, these findings of local sleep occurring in restricted cortical circuits provide a most plausible neurophysiological explanation for the performance deficits that can occur in conditions of restricted sleep and tiredness, and that are the cause for many accidents.
Regarding the study by Ferrie et al., as I see it, this study shows that impaired cognitive functions are observed more often in people who, over the 5.4-year study period, changed their reported average sleep duration (during weekdays) from six to eight hours to either a longer sleep duration or a shorter one. In the past, quite a number of studies have shown a link between sleep duration and cognitive function. However, this study is unique in that it focuses on the significance of changes in habitual sleep duration. Unfortunately, this study reported sleep duration assessed in the beginning and at the end of the approximately five-year study period, whereas cognitive function was assessed only at the end. Thus, we do not actually know whether the participants with substantial changes in sleep duration did, or did not, have decreased cognitive function already in the beginning of the study period. If participants having “normal” sleep duration in the beginning of the five-year period had also normal cognitive function at this time, and cognitive function during the five-year period changed in parallel with change in sleep duration, then the data would corroborate the view that sleep plays a highly important role for the development and maintenance of cognitive functioning during later life. However, the implications of the study would obviously be different if cognitive performance was already in decline at the beginning of the study.
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