Neurophysiology of Sleep - Essay Example

Running head: Neurophysiology of sleep Neurophysiology of sleep [The of the appears here] [The of appears here] Neurophysiology of sleep It is thought that for cerebral representations to be modified or updated, the cells over the whole cerebral cortex should become modifiable, and that at such times ordinary information (from the external environment) should be rigorously excluded. The time when such a condition normally exists is during sleep. During sleep, the cerebral EEG periodically alternates between desynchronization (D sleep) and synchronization (S sleep). Correspondent with these EEG changes is a periodic alternation between sleep with rapid eye movements (REM sleep) and sleep without rapid eye movements. It is thought that mental activity takes place during D/REM and S/NREM sleep, but that the mental activity during D/REM sleep is the most dream-like, while that occurring during S/NREM sleep is much more awake-like. Consequently, it is the D/REM sleep phase that is thought to be correspondent with the actual experience of dreaming, while the subsequent S/NREM phase is correspondent with mental activity related to the experience of the preceding dream phase. (Marjorie L. Rand, 2002) Normally, dream sleep appears at 70-90 minute intervals throughout the sleep period in adults. There is, however, evidence that the physiological and neurophysiological activity normally correspondent with dream sleep also occurs with the same periodicity, but less intensely or evidently, throughout the awake state. Underlying the two psychological systems considered to interact during the process of dreaming may be two physiological or neuroanatomical systems. Dream sleep may involve the preponderant or emergent activity of a neuroanatomical region different from the region that normally is preponderantly active in the awake state. (Cheryl H. Alexander, 2000). One factor thought to contribute to the onset of sleep, particularly dream sleep, is a reduction of externally generated stimuli that reach the higher and conscious level of the brain. As a result of this reduction there may be facilitated a release of internally generated past impressions or memories from within the lower neuroanatomical and unconscious levels. Within the higher, or cerebral, level of the brain, the emergence of information released from the lower level may also involve a decreased activity of processes, or switching off of the system that would normally in the awake state inhibit such preponderant emergence. (Edmund T. Rolls, 2000). Relative to the S/NREM sleep phase, the D/REM sleep phase is accompanied by increased cerebral blood flow; increased activity of the autonomic nervous system; increased "spontaneous" activity of the reticular formation; a higher response threshold in the midbrain reticular formation to auditory as well as direct stimulation; and a higher threshold for behavioral awakening. (Simon J. Sherwood, 2002). Among the phenomena evident during D/REM sleep are cerebral desynchronization; hippocampal theta waves of 5-6 Hertz, a depression of spontaneous and reflex activity in the muscles and a general atonia, especially of the antigravity muscles. The preceding phenomena constitute a tonic background on which are superimposed the following phasic phenomena: large amplitude waves occurring in the pontine reticular formation, lateral geniculate nuclei and occipital cortex, which are referred to as PGO activity and which normally occur coincidentally with REM bursts; short-term increases in the frequency of the hippocampal theta rhythm; increased muscle activity and myoclonic twitches; and short fluctuations within the autonomic nervous system. Also involved in D/REM sleep are the parietal lobe, the temporal lobe, the cerebral limbic regions, and the pulvinar of the thalamus. (Elena Miro, M. Carmen Cano, Lourdes Espinosa-Fernandez, Gualberto Buela-Casal, 2003). Both the tonic and phasic phenomena of dream sleep may be regarded basically as an ascending excitatory component involving activity of the cerebral cortex and ascending sensory systems (reticular and PGO activity), and a desynchronizing component that is largely inhibitory. (Michael P. McQuillen (2005) Ascending Component The most frequently described route for REM-related ascending impulses traveling to the cerebral cortex is from the pontine brain stem to the lateral geniculate nucleus and thence to the occipital cortex. Input to the lateral geniculate, as evidenced in part by the PGO activity, is not from the eye muscle afferents or retina; that is, it does not first descend to the pontine region and then ascend from there: It travels only in an ascending direction from the pontine region. It is thought that, of the phasic phenomena of D/REM sleep, the PGO spikes in particular reflect the neurological activity underlying the experience of dreaming. (Martin B. Keller, 2003) Descending Component There are thought to be two inhibitory processes acting on motor output during sleep. There is atonic depression which lasts throughout the sleep episode, and there is a phasic depression, or enhancement of depression, which occurs synchronously with the bursts of REM or PGO activity during dream sleep. Despite the phasic depression, there are muscular twitches during the REM bursts. These twitches are thought to occur whenever the excitatory volley that accompanies the REM burst is strong enough to overwhelm the inhibitory impulses. Phasic increases of excitatory output synchronous with REM bursts are evident in the pyramidal system, the mesencephalic reticular formation, and the red nucleus, and may contribute to the muscular twitches. The phasic inhibitory output appears to particularly involve the vestibular nuclei. It is thought that the predominance of inhibition upon the motor system during dream sleep prevents the motor execution of a behavioral response to (or within) the internally generated stimuli of the dream. (Adam Zeman, Tom Britton, Neil Douglas, Andrew Hansen, Jane Hicks, Robin Howard, Andrew Meredith, Ian Smith, Gregory Stores, Sue Wilson, and Zenobia Zaiwalla, 2004) The Cellular Electrophysiology of Sleep Most of our knowledge about the cellular basis of sleep over the last forty years has been gained from recording the electrical activity of single neurons. The very first studies showed that, contrary to expectations, single neurons in the cerebral cortex do not stop firing during sleep. The spontaneous rate of firing is only slightly lower in non-REM sleep than in waking, and it is often higher in REM sleep. For most cortical neurons, the simpleminded hypothesis that sleep provides rest by mere inactivity, as relaxation does for muscle cells, is untenable. Several aspects of neural activity, however, differ markedly between waking and sleep. These differences have been studied in recent years by examining the thalamocortical system. (Ilia J. Elenkov, Ronald L. Wilder, George P. Chrousos, and E. Sylvester Vizi, 2000) Sensory information impinging upon the cerebral cortex is funneled through the thalamus. During waking, neurons in the brain stem reticular formation exert an excitatory influence on neurons in the thalamus. Consequently, the membrane potential is kept in a state of relative depolarization, and activated nerve cells discharge tonically in single spikes. After sleep onset, the activating influence of brain stem reticular neurons diminishes and as a result the membrane potential of thalamic and cortical neurons becomes more negative. Due to this hyper polarization, both thalamic and cortical neurons generate repetitive burst discharges followed by long pauses during which their membrane potential is very negative. The ability of neurons to respond to extrinsic stimuli is reduced. This results in the disconnection of the brain's intrinsic activity from outside events. How do these cellular changes in the brain relate to the EEG pattern that is recorded from the scalp A fascinating new result is that the membrane potential of thalamocortical neurons and the cortical EEG exhibit similar fluctuations. As sleep deepens the nerve cells in the thalamus become increasingly hyperpolarized, with fluctuations in their membrane potentials occurring first in the frequency range of the sleep spindles and then in the range of slow waves. The same typical sequence of changes is seen in the EEG as non-REM sleep progresses from a superficial stage that is characterized by the periodic occurrence of sleep spindles to deep sleep, where slow waves predominate. Recently, an even slower rhythm with a frequency below 1 Hz was described at the cellular level and then discovered also in the EEG. These new developments are important for sleep research because they make it possible to identify the neurophysiological mechanisms underlying the sleep EEG. (Lee M. Miller and Christoph E. Schreiner, 2000). Not all neurons exhibit the typical low firing rate during non-REM sleep and a high firing rate during REM sleep. A few cell groups in the brain stem reduce their activity in non-REM sleep and become almost silent in REM sleep. These particular neurons send diffuse projections to the entire brain, influencing their targets by releasing the neuromodulators norepinephrine, serotonin, or histamine. For example, the noradrenergic neurons in the locus coeruleus and the serotoninergic neurons in the raphe system fire tonically during waking, discharge at much lower levels during non-REM sleep, and cease firing during REM sleep. These neurons typically discharge in a transient, phasic manner whenever the animal encounters a salient event. This modulation is lost during sleep. The distinctive firing pattern of these neurons indicates that they may be closely associated with the behavioral state of the animal. Reference: Adam Zeman, Tom Britton, Neil Douglas, Andrew Hansen, Jane Hicks, Robin Howard, Andrew Meredith, Ian Smith, Gregory Stores, Sue Wilson, and Zenobia Zaiwalla (2004). Narcolepsy and excessive daytime sleepiness; BMJ Cheryl H. Alexander (2000). Neurophysiological and Psychological Assessment of an Individual Experiencing Anomalous Mental Phenomena: A Second Case Study; The Journal of Parapsychology, Vol. 64 Edmund T. Rolls (2000). Memory Systems in the Brain; Annual Review of Psychology Elena Miro, M. Carmen Cano, Lourdes Espinosa-Fernandez, Gualberto Buela-Casal (2003). Time Estimation during Prolonged Sleep Deprivation and Its Relation to Activation Measures; Human Factors, Vol. 45 Ilia J. Elenkov, Ronald L. Wilder, George P. Chrousos, and E. Sylvester Vizi (2000).The Sympathetic Nerve An Integrative Interface between Two Super systems: The Brain and the Immune System; Pharmacol Rev J. Moore (2002). Some Thoughts on the Relation between Behavior Analysis and Behavioral Neuroscience; The Psychological Record, Vol. 52 Lee M. Miller and Christoph E. Schreiner (2000). Stimulus-Based State Control in the Thalamocortical System; J. Neurosci Marjorie L. Rand (2002). Mirror Neurons: Somatic Empathy and Countertransference; Annals of the American Psychotherapy Association, Vol. 5 Martin B. Keller (2003). Past, Present, and Future Directions for Defining Optimal Treatment Outcome in Depression: Remission and Beyond; JAMA Michael P. McQuillen (2005). Electrodiagnosis in Clinical Neurology; JAMA, September 7 Simon J. Sherwood (2002). Relationship between the Hypnagogic/hypnopompic States and Reports of Anomalous Experiences; The Journal of Parapsychology, Vol. 66 Read More