How and why do we sleep, why do we dream?

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Sarah Messenger (0801595)                                                               SJPS5004

How and why do we sleep, why do we dream?

Considering the functions of sleep and dreams, it has been suggested that humans spend approximately one third of their lives asleep (cited in Goldsmith, 2005). However, there still remains no clear agreement on what the function of sleep is. This essay focuses on exploring how humans sleep, and possible explanations for why we sleep and why we dream.

It is believed that sleep follows a circadian rhythm, effecting sleep onset and stages (cited in Sanei & Chambers, 2007). The human biological circadian rhythm is roughly a 24 hour cycle, which is controlled by a circadian pacemaker. This "pacemaker" is the section of the brain known as the suprachiasmatic nucleus (SCN), which is situated in the hypothalamus (cited in Stickgold & Walker, 2009).

Signals produced by the SCN travel to different regions of the brain which controls the sleep-wake cycle within humans (cited in Kramer et al, 2001). The SCN regulates other functions associated with the sleep cycle such as body temperature, hormone secretion, urine production, and changes in blood pressure, which are all known to decrease during the sleep process. The SCN controls and is entrained to the sleep-wake cycle which is dependent on the cycle of light and dark, and on body temperature. A change in these could shift or disrupt the cycle.

One internal factor affecting the circadian rhythm is melatonin (cited in Bermudez, Forbes & Indiji, 1983). The SCN regulates the pineal gland’s secretion of melatonin, which has a day/night function. Melatonin is a hormone that helps to regulate sleep. The release of melatonin is dependent on the availability of light on the ganglion cells which contain the photopigment melanopsin. The ganglion cells receive light information through receptors known as rods and cones. This information travels along the retinohypothalamic pathway, where the SCN receives and interprets the environmental light, which determines the release of melatonin (cited in Hannibal & Fahrenkrug, 2002). Peak levels of melatonin arise in the darkness at night when the release of melatonin is not suppressed. The lowest levels of melatonin arise in daylight, when the suppression of melatonin occurs due to the availability of light. This process allows the body to sleep effectively at night, and wake in the day (cited in Olive, 2006).

The importance of melatonin in the process of sleep is emphasised in a study carried out by Czeisler et al in 1995. This study looked into the effects of light and melatonin in blind people. The findings indicated that, in general, most blind people are not entrained to a 24-hour day, and tend to suffer from sleeping disorders such as insomnia in spite of sleep, work and social contact. One of the suggestions for this is that due to blind people having a limited exposure to light, melatonin is not suppressed during the day. This leads to a dysfunction in the 24-hour cycle which can possibly lead to sleep disorders.

External factors that affect the circadian rhythm are called zeitgebers. A zeitgeber is an external cue which influences the operations of the internal clock in humans (cited in Smith, Comella & Hogl, 2008). One of the most powerful zeitgebers is light, which is known as an ‘exogenous zeitgeber’; a natural cue to influence the sleep-wake cycle in humans. However, a study by Aschoff and Weber (cited in Kleitman, 1963), used an underground bunker, where student participants were allocated to stay for a period of time. Although the participants did not have any cues to light, they were still found to settle into a regular sleep-wake cycle of approximately 25-27 hours. The results of this suggest that humans may have internal mechanisms to influence the pattern of sleep. It is suggested therefore that humans possess some form of a natural alarm clock, which can trigger a human’s internal clock, such as an internal cue to eat, wake or make an important meeting (cited in Grondin, 2008).

The way in which humans sleep has been observable since the introduction of the electroencephalograph (EEG). The EEG, introduced by Berger in 1929 (cited in Smith, Van Gils & Prior, 2006), records the electrical activity of billions of cortical neurons using a number of small metal electrodes on the surface of the skull. The electro- oculography (EOG), measures eye movement, whereas the electromyography (EMG), measure muscle tension.  This non-invasive procedure can be ‘synchronised’ with a repeated and recognisable waveform, or ‘desynchronised’, with an apparently random pattern of spikes and waves, where there is no consistent waveform. The EEG has a number or frequency of spikes or waves per second, which is measured as cycles per second, known as herz (Hz).

Aserinksy and Kleitman in 1953 (cited in Siegel, 2002), concluded that there are two distinct stages of sleep; ‘slow-wave’ sleep (SWS) and ‘rapid eye movement’ sleep (REM).  

There are believed to be four stages of SWS (cited in Sircar, 2008). In stage one, the EEG pattern demonstrates ‘theta waves’, with a frequency of 4 to 7 Hz. Stage two occurs approximately ten minutes after this, where the EEG pattern becomes synchronised with slower and larger waves which are interrupted by bursts of fast spiking activity, known as the ‘sleep spindles’, with a frequency of 12 to 16 Hz. Stage three of SWS is dominated by large ‘delta waves’ with a frequency if 1 to 3 Hz, with sleep spindles becoming less common. Heart rate, respiration, metabolic rate and body temperature continue to fall at this stage. In stage four, the EEG recording consists only of delta waves, with a remaining frequency of 1 to 3 Hz. At this stage, metabolic rate is at its lowest. The arousal threshold (a measure how difficult it is to wake an individual from sleep) is very high.

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Sleep is believed to be a dynamic process; after approximately 30 minutes in stage four of SWS, it is suggested that humans ascend through the sleep stages to the light SWS of stage two (cited in Hobson, 1994). At this point, approximately 90 minutes after going to sleep, the EEG activity suddenly shifts into the fast, desynchronised pattern of the aroused person. This stage of sleep is known as ‘rapid eye movement’ sleep (REM) (cited in Bear, Connors & Paradiso, 2007).  

At the point where an individual reaches REM sleep, arousal thresholds are very high and the skeletal muscles ...

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