Our main sleep research topics focus on brain plasticity and cognition during sleep. For cognition during sleep, please also see the “disorders of consciousness” (DOC) project.
Why do we sleep?
On average, one third of our lives pass by in sleep. Sleep and wakefulness like many behaviours and physiological processes (e.g., body temperature, blood flow and hormone levels) follow a 24 hours circadian rhythm. Those rhythms are endogenous and can persist without environmental cues, requiring an internal “pacemaker”- namely the suprachiasmatic nucleus of the anterior hypothalamus. However, under normal circumstances circadian rhythms are additionally modulated by external timing cues (“Zeitgeber”) like sunlight that adapt the rhythm to the environment. Sunlight is linked to the active phase of the circadian rhythm in some mammals and the inactive phase in others. Thus, most adult humans sleep at night when it is dark, whereas nocturnal animals such as rats and bats sleep mostly when it is light. All mammals, birds and reptiles appear to sleep, whereas sleep duration varies widely from about 18 hours a day in bats and opossums to about 3 hours a day in horses and giraffes (Bear, Connors, & Paradiso, 2001). So far the functions of sleep still remain largely unknown despite our understanding of the processes generating and maintaining sleep are rapidly increasing. It is still discussed whether sleep is necessary to the whole body or whether particular organs – among which is the brain – are the primary targets of the sleep processes. Numerous hypotheses have been proposed for sleep function, however, the main functions of sleep might be energy conservation, regeneration, information processing (learning and memory processes) and development (language, motor skills, maturation of the brain).
Probably the most important theory of sleep regulation is the two-process model by Borbély (1982). According to this model, both the homeostatic sleep pressure (process S) and a circadian process (process C) are responsible for sleep regulation. While the circadian process is based on an “internal clock”, which ensures that we get sleepy at about the same time every day, the sleep pressure depends on the extent of previous wakefulness. A disturbance of this interaction can lead to daytime sleepiness, sleep problems and reduced cognitive performance during the day.
Sleep is usually operationalized and studied by means of polysomnography (PSG), which is a combination of electroencephalography (EEG), electrooculography, electrocardiography (ECG) and electromyography (EMG). With PSG measures such as sleep architecture, latency to sleep onset, total sleep time, number of arousals and awakenings and sleep efficiency are routinely calculated to characterize a night of sleep. It are disturbances in those measures which objectively verify complaints of difficulty initiating or maintaining sleep. Furthermore, it is the only way to differentiate physiologically-based sleep disturbances from sleep state misperception, that is, patients having the complaint of insomnia in the absence of objective findings from polysomnography.
As PSG recordings show, sleep has distinct phases. During a normal night, humans usually cycle through non-rapid eye movement (NREM) and rapid eye movement (REM) sleep stages.
According to Rechtschaffen and Kales (1968) sleep was classified in waking, movement time, four NREM sleep stages and REM-sleep. In 2007 the American Academy of Sleep Medicine (AASM) published revised guidelines for the scoring of sleep and associated events. They combined stages 3 and 4 into one stage 3 and eliminated movement time, therefore only four stages remained: Three non-REM stages (N1, N2, N3, with increasing sleep depth) and one REM stage (R). Sleep stages are thereby classified by PSG and are usually staged in 30 second epochs.
Stage 1 (N1) is the phase where we fall asleep. It is a very light sleep, in which mainly slow waves occur (theta waves in the range between 2 and 7 Hertz, no K-complexes or sleep spindles).
Stage 2 (N2) is characterized by certain EEG patterns, so-called sleep spindles and K complexes. N2 is mainly light sleep with a small amount of slow waves (delta waves from 0.5 to 2 Hertz). This stage accounts for about 50% of the night.
Stage 3 (N3) is known as deep sleep and mainly consists of slow waves (delta waves).
REM sleep (Rapid Eye Movement) sleep or dream or paradoxical sleep is characterized by similar brain activity as in the waking state, whereas the muscle activity is very low, so we can´t act out our dreams.
Within the first half of the night deep sleep predominates, whereas in the second half of the night a greater proportion of REM sleep occurs.
Approximately 25% of the population suffers from sleep problems, with women being affected more often than men. According to the International Classification of Sleep Disorders (Thorpy, 1990) the main categories of sleep disorders are:
- Dyssomnias: Difficulty initiating or maintaining sleep or excessive sleepiness.
- Parasomnias: The parasomnias are disorders that appear during sleep. Examples are sleepwalking, sleep talking, nightmares and bruxism.
- Sleep disorders associated with mental, neurologic, or other medical disorders such as migraine, Parkinson’s disease, chronic pain, thyroid disease, depression and anxiety.
Causes of sleep disorders can be psycho reactive load factors (e.g., anger, worry), psychosocial aspects (e.g., family problems, job loss), exogenous events (e.g., sleep environment, day-night shift), climatic and meteorological factors (e.g., heat, change in the weather) and organic causes (e.g., organic diseases, substance abuse, depression).
Bear, M. F., Connors, B. W., & Paradiso, M. A. (2001). Neuroscience: Exploring the brain: Lippincott Williams & Wilkins.
Borbély, A. A. (1982). A two process model of sleep regulation. Human neurobiology, 1(3), 195-204.
Borbély, A. A., & Achermann, P. (2000). Homeostasis of human sleep and models of sleep regulation. In M. H. Kryger, T. Roth & W. C. Dement (Eds.), Principles and practice of sleep medicine (pp. 377–390). Philadelphia: WB Saunders Co.
Thorpy, M. J. (1990). The international classification of sleep disorders: diagnostic and coding manual: American sleep disorders association.
Sleep and gross motor learning in school aged children and adults
The functional role of sleep in memory consolidation has already been shown several times. Convincing findings exist which suggest that sleep is primarily necessary for consolidation of procedural memory (learning of skills like e.g. driving a car) – especially for encoding motor processes. So far mainly the impact of sleep on fine motor skills such as mirror tracing, finger tapping or pursuit rotor has been studied. With this project the relationship between sleep and learning of a gross motor task (riding an inverse steering bike) is studied for the first time. It is believed that sleep as compared to sleep deprivation will lead to an improvement of motor performance.
The role of memory strength for processes of sleep-associated memory consolidation
While recent findings demonstrate that processes of sleep-associated memory consolidation can stabilize memories, it is largely unclear whether such consolidation varies with one of the most basic features of memory representations, i.e., memories initial strength. The aim of this project is to fill this empirical gap by examining the role of memory strength for memory consolidation. Across a row of experiments, memory strength will be manipulated using intentional and incidental encoding procedures. Effects of memory consolidation will be measured via investigations of time-dependent forgetting and memories interference susceptibility. Furthermore, electroencephalography will be used to study how manipulations of encoding strength change the neural correlates of initial memory formation and change retrieval processing right after encoding as well as following a period of sleep or wakefulness. In addition, sleep EEG will be employed to examine sleep mechanisms believed to be directly involved in the reactivation and restructuring of newly formed memories. The results will provide a first overall picture on the role of memory strength for sleep-associated memory consolidation.