Biology of Sleep essay

Sleep is a universal characteristic demonstrated in every animal species studies, from mammals to insects. As such, it forms one of the most paramount human behaviors that occupy roughly one third of the human lives. Despite the fact that the function of sleep is still unknown, it is necessary for survival as prolonged sleep deprivation results to severe physical, as well as, cognitive impairment, and finally death. Tentatively, sleep is relevant to medicine since sleep disturbance happens in virtually all psychiatric illness and are in most cases part of the diagnostic criteria for disorders (Martins, 2011). Undoubtedly, sleep has a relative unconsciousness of the external worlds as well as a general lack of memory of the state, unlike people who have been comatose, sleep forms as a termination of an episode.

For research, as well as, clinical purposes, sleep illustrates by the combination of behavioral observation with electrophysiological recording. Human, like other mammals, present two types of sleep: rapid eye movement (REM) and non-rapid eye movement (NREM) sleep. As such, this state has distinctive psychophysiological as well as neurophysiological traits. REM sleep derives its name from the frequent bursts of the eye movement activity that happens. Tentatively, REM also known as paradoxical sleep since the electroencephalogram during sleep is comparable to that of waking. Certainly, the equivalent of REM sleep referred to as active sleep of prominent phasic muscle shifts. On the other hand, NREM sleep or orthodox sleep has the characteristic of reduced activation of the EEG, as such, its name quiet sleep since it lacks the relative motor activity.

Stages of sleep

Within REM and NREM sleep, there exists further classification known as stages. Sleep typically scores in epochs of 30 seconds with stages of sleep defined by the visual scoring of three parameters: EEG, electrooculogram (EOG), as well as, electromyogram (EMG0 recorded beneath the chin. In the wakefulness process, the EEG exhibits a low voltage fats activity or activated pattern. As such, voluntary eye movements, as well as, eye blinks are dominant. Tentatively, EMG has a relatively high tonic activity with additional; phasic related activity to voluntary movements. In the case when the eyes closed in sleep preparation, alpha activity (8-13 cycles per second) becomes prominent, especially in occipital regions. NREM sleep divides into four stages. Sleep enters through a transitional stage, stage 1 sleep, characterized by loss of alpha activity as well as appearance of low voltage mixed frequency EEG pattern that has prominent theta activity (3-7 CPS) (Oliveira, 1996). Additionally, it has occasional vertex sharp waves. As such, the eye movement becomes slow and rolling as well as the skeletal muscles tone relaxes. In most cases, stage 1 is not sleeping although there occurs reduced awareness of the sensory stimuli, especially visual and mental activity becomes more dreams like.

As such, the motor activity may persist in the first number of seconds during stage 1. As such, individuals sometimes accompanied by sudden muscle a contraction that has a sense of falling and/or dreamlike imagery, these hypnotic jerks are benign and may be exaggerated by sleep deprivation. After several minutes of stage 1, sleep always undergoes stage 2.Heralded by the appearance of sleep spindles (12-14 CPS, as well as k-complex in the EEG), this stage is succeeding stages of REM, as well as, NREM sleep are all subjectively referred to as sleep(Oliveira, 1996).

Arguably, at the beginning of the night, stage 2 supplements by a period that comprises of stages 3 and 4. Tentatively, slow waves appear during these stages that subdivided according to the delta proportion waves in the epoch: stage 3 needs a minimum of 20 % and not more than 50 % epoch time occupied by a slow wave activity (Oliveira, 1996). As such, the stages, 3 and 4 called slow wave sleep, delta sleep or deep sleep, as arousal threshold augments from stages 1 through to stage 4.The movements of the eyes during stages 2-4 and EMG activity decrease further (Oliveira, 1996). REM sleep does not subdivide into stages but rather defined in terms of tonic as well as phasic components. As such, tonic stage of REM sleep comprises the activated EEG similar to that of stage 1 that may exhibit augmented activity in the theta bands, as well as, a generalized atonia of skeletal muscles except for the extraocular muscles and the diaphragm. Undoubtedly, the phasic features of REM include irregular burst of rapid eye movements as well as muscles twitches.

Sleep organization

The amount of sleep obtained during the nights varies across different people as some people may require 7-9 hours functioning optimally. Nonetheless, there exist short sleeper hours that seem to operate adequately with less than 6 hours per night, as well as long sleepers who may require 12 or more hours to sleep (Oliveira, 1996). In addition, a to the genetic factors that influence daily sleep requirements, age as well as medical or psychiatric disorders also strongly affect the sleep patterns (Martins, 2011). As such, regardless of hours needed to sleep, the proportion of the time spent in the subsequent stages as well as the patterns of stages across the night is fairly consistent in normal adults. As such, a healthy young Med 1 will need about 5% of the sleep period in stage 1 sleep, about 55% in the second stage, 25 % in each of SWS as well as REM sleep (Oliveira, 1996).

Certainly, sleep happens in cycles of NREM-REM sleep that last approximately 90-110 minutes. The stages Stages 3 and stage 4 (SWS) forms the prominent early in the night, especially during the initial NREM period and diminishes as the night advances. As SWS wanes, a period of REM sleep as well lengthens, whilst revealing greater phasic activity as well as, more forceful dreaming later in the night.

Circulatory and Neurotransmitters underlying Wakefulness, NREM and REM sleep Wakefulness

Wakefulness associates itself with a low-voltage frequency EEG known as activated or desynchronized. As such, the ascending reticular activating system maintains an activated EEG. Ascending projections from the medulla, Pons, as well as midbrain travel in the ARAS arise from cholinergic cell groups in the Pons referred to as lateral dorsal tegmental, pedunculopontine tegmental and nucleus reticularis pontis. On the other hand, other ascending axons arise from serotonergic cell groups at the mid brains Pons junction, the dorsal raphe as well as medulla. Additionally, another contribution to the system is the augmenting axons that arise from the cell that contain the norepinephrine ; the cells are in locus coeruleus as well as medulla. A final member of the ascending activating system compares to axons of dopaminergic cells in the substantia Nigra pars compacta as well as ventral tegmental area.

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Non REM sleep

The non REMM sleep initiates with the emergence of inhibitory signals that arise from the ventrolaterally preoptic area. As such, this area lays just rostalm to the optic chiasm. VLPO neurons, on the other hand, are active sleeping in that they augment their discharge selectively at the onset of sleep. Thus, the VLPO cells contain the GABA as well as the project to serotonergic, noradrenergic as well as cholinergic cell group in the brain stem reticular formation as well as histaminergic population in the TM that is posterior /caudal hypothalamus. These neurons in the brain stem present the reduction in the activity across sleep stages as VLPO neurons show the progressive activation. Thus, activation of VLPO neurons induces the inhibition of the wake promoting neuronal cells linked with the ARA. Undoubtedly, the brain stem feedback and inhibition the VLPO sleep promoting neurons. Therefore, a sleeping process that starts with the activation of the VLPO inhibits the wake promoting systems that could remove VLPO neurons inhibition. Thus, the inhibition of the neurons forms the onset of the sleeping process.

A poignant input mediated by the wake promoting neurons inhibits VLPO neurons that would then remove inhibition from wake promoting neurons. Thus, the system can switch decisively between sleep as well as waking and also be inclined to maintain continued sleep as well as weak states. On the other hand, adenosine has long been known to be sleep promoting as well as its effect blocked by caffeine. Thus, it is reasonable to anticipate that adenosine is sleep factors that indirectly or directly normalize the VLPO neuron activity.

REM sleep

The EGG of REM sleep resembles the EEG of active wakefulness, and in some species they are virtually indistinguishable. Arguably, considering that these two states could not be more varied in their behavioral characteristics. Thus, the phasic as well as tonic REM sleep often distinguished. Phasic REM sleep events are persistent. As such, there exists a flaccid paralysis of radical groups of muscles. As such, the muscles involved in REM sleep generation lies primarily in the Pons. The cholinergic neurons in the nucleus reticularis pontis partake, in REM sleep generation, via their projection to cortex as well as thalami. Additionally, the cells in the DR as well as LC prevent the cholinergic cells in reicularis pontis during waking as well as NREM sleep. Thus, the transition between REM and NRE sleep thought to rely upon GABA-ergic inhibition of LC as well as DR that no longer inhibit reticular is pontis. When the GABA cells stops stop firing, NTREM returns and wakefulness occurs when the sensory stimulation happens, and the ARAS starts. The cholinergic neutrons in the reticularis pontis have descended projections to the brain stem as well as spinal cord that prevent the tonic REM phase.

Physiological Changes Associated with Sleep

During NREM sleep as well as tonic REM sleep, there exist s relative augment in parasympathetic activity relative to sympathetic activity. As such, the autonomic nervous system reaches its most stable state during SWS in comparison to wakefulness. Thus, during the phasic TREM sleep, there exist brief surges in parasympathetic as well as sympathetic activities that result in a high autonomic instability degree. On the other hand, cardiac output, hear rate as well as blood pressure decrease during NREM sleep, thus reaching their lowest possible values and the least vulnerability in SWS. Nonetheless, theses strictures remain reduced on average during REM sleep with retrospect to waking, they attain their peak values during REM. Temporary breathing instability, as well as, periodic breathing happens on the onset of sleeping process(Lopes, 1998). Additionally, the respiratory rate, as well as minute ventilation, reduces during the sleeping process, and the upper airway resistant augment due to muscle relaxation, most considerably during REM sleep. As such, these changes contribute to exacerbations of the underplaying pulmonary disease and sleep related breathing disorders like sleep apnea (Martins, 2011).

The brains, as well as the body temperature regulated during NREM sleep, particularly SWS, experienced as a result of a decreased hypothalamic activity set point as well as active heat loss (Lopes, 1998). As such, individuals commonly experience these phenomena when they go to deep feeling somewhat cold and wake up hours later to throw off the supplemented covers. Thus during REM there is an experience in decreasing ability in body temperature regulation through sweating, as well as, shivering (Lopes, 1998).

The growth hormone, on the other hand, ejects in the early parts of the night and its secretion enhanced by SWS. Additionally, sleep stimulated prolactin section, during the middle portion of the night.

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