The importance of sleep for maintaining good health is increasingly recognized. Sleep disturbances have potentially serious adverse effects: epidemiological studies show that sleep disturbances are associated with a number of conditions, including depression, anxiety, and alcohol and drug abuse (Katz and McHorney Citation1998; Ohayon and Zulley Citation2001; Okuji et al. Citation2002; Taylor et al. Citation2003). Insomnia is also associated with reduced immune function (Taylor et al. Citation2003) and a possible association with cardiovascular disease and hypertension has been postulated (Katz and McHorney Citation1998; Vgontzas et al. Citation2009).
Slow-wave sleep (SWS) refers to stages 3 and 4 of nonREM sleep. During these sleep stages the EEG is dominated by low frequency, high amplitude oscillations which can be quantified by visual inspection of the EEG. The slow oscillations in the EEG can also be quantified by signal analysis based methods such as spectral analysis and this result in a measure called slow-wave activity (SWA).
The slow waves in the EEG reflect the synchronous slow oscillations of many cortical neurons. During the slow oscillation, a period of hyperpolarization during which no action potentials are observed, alternates with a phase of depolarization during which a burst of action potentials occur (Crunelli and Hughes Citation2009).
It is very well established that SWS is regulated accurately in relation to the duration and intensity of wakefulness and sleep. This accurate regulation is observed in humans and other mammals and implies that SWS is an essential part of the sleep process and its restorative functions. The precise mechanisms underlying the precise regulation of SWS as well as the mechanisms by which SWS contributes to the restoration which takes place during sleep, are not well understood.
One current hypothesis is that the increase in SWS in response to increased duration of wakefulness reflects the increase in synaptic strength in neuronal networks, as well as an increase in sleep regulatory substances in response to waking activity (Tononi and Cirelli Citation2006; Krueger et al. Citation2008).
The putative role of SWS is to reverse some of these wake dependent changes, e.g., SWS has a role in maintaining synaptic homeostasis (Tononi and Cirelli Citation2006), or “synaptic super structure” (Krueger and Obal Citation1993; Krueger and Obal Citation2003).
In the first review article, Pierre-Hervé Luppi discusses the mechanisms by which the transitions between the three vigilance states, namely waking, nonREM sleep and REM sleep occur over a 24-h period (Luppi Citation2010). Recent insights into the mechanisms through which cortical activity switches from an activated state during waking to a synchronized state during nonREM sleep are presented. Multiple hypothalamic and brainstem systems are understood to be involved in cortical activation during the waking process and the dissipation of activation during SWS, and these are discussed.
Recent advances in imaging techniques used to investigate the changes that occur in brain activity during waking and nonREM and REM sleep are discussed by Pierre Maquet (Maquet Citation2010). NonREM sleep was previously thought to be a period of brain quiescence due to the loss of consciousness and low response to external stimuli observed during this period. However, newer imaging techniques in which the imaging is synchronized to the phase of the slow oscillation and the occurrence of sleep spindles, suggest that nonREM sleep is in part a highly active state.
The evidence for a central role of SWS in the consolidation of declarative memory is discussed by Jan Born in the third article (Born Citation2010). According to one conceptual model reactivation of encoded memories in the hippocampus during SWS stimulates the transfer of reactivated memory to the neocortex for long-term storage.
Lastly, the contribution of SWS and SWA to sleep maintenance, the recovery processes that occur during sleep and present evidence for SWS deficiency in insomnia and other psychological disorders is explored (Dijk Citation2010). Some emerging data on pharmacological agents that enhance SWS and SWA are presented and their effects on other sleep parameters are discussed.
This collection of articles is based on the presentations given at the symposium “Pharmacological intervention in slow-wave sleep – A novel approach to the management of insomnia” during the 9th World Congress of Biological Psychiatry, Paris, 2009. These articles will hopefully provide the reader with an informative overview of the importance of SWS and how recent findings on the function of SWS may aid the development of future treatments of insomnia.
References
- Born J. 2010. Slow-wave sleep and the consolidation of long-term memory. World J Biol Psychiatry 11 (Suppl 1):16–21.
- Crunelli V, Hughes SW. 2009. The slow (<1 Hz) rhythm of non-REM sleep: a dialogue between three cardinal oscillators. Nat Neurosci 13(1):9–17.
- Dijk DJ. 2010. Slow-wave sleep deficiency and enhancement: implications for insomnia and its management. World J Biol Psychiatry 11 (Suppl 1):22–28.
- Katz DA, McHorney CA. 1998. Clinical correlates of insomnia in patients with chronic illness. Arch Intern Med 158(10):1099–1107.
- Krueger JM, Obal F. 1993. A neuronal group theory of sleep function. J Sleep Res 2(2):63–69.
- Krueger JM, Obal F Jr. 2003. Sleep function. Front Biosci 8:d511–519.
- Krueger JM, Rector DM, Roy S, Van Dongen HP, Belenky G, Panksepp J. 2008. Sleep as a fundamental property of neuronal assemblies. Nat Rev Neurosci 9(12):910–919.
- Luppi PH. 2010. Neurochemical aspects of sleep regulation with specific focus on slow-wave sleep. World J Biol Psychiatry 11 (Suppl 1):4–8.
- Maquet P. 2010. Understanding slow-wave sleep through neuroimaging. World J Biol Psychiatry 11 (Suppl 1):9–15.
- Ohayon MM, Zulley J. 2001. Correlates of global sleep dissatisfaction in the German population. Sleep 24(7):780–787.
- Okuji Y, Matsuura M, Kawasaki N, Kometani S, Shimoyama T, Sato M, . 2002. Prevalence of insomnia in various psychiatric diagnostic categories. Psychiatry Clin Neurosci 56(3):239–240.
- Taylor DJ, Lichstein KL, Durrence HH. 2003. Insomnia as a health risk factor. Behav Sleep Med 1(4):227–247.
- Tononi G, Cirelli C. 2006. Sleep function and synaptic homeostasis. Sleep Med Rev 10(1):49–62.
- Vgontzas AN, Liao D, Bixler EO, Chrousos GP, Vela-Bueno A. 2009. Insomnia with objective short sleep duration is associated with a high risk for hypertension. Sleep 32(4):491–497.