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(physical chemistry) a sample of matter in which substances in different phases are in equilibrium; "in a static system oil cannot be replaced by water on a surface"; "a system generating hydrogen peroxide"
instrumentality that combines interrelated interacting artifacts designed to work as a coherent entity; "he bought a new stereo system"; "the system consists of a motor and a small computer"
a group of independent but interrelated elements comprising a unified whole; "a vast system of production and distribution and consumption keep the country going" (同)scheme
a complex of methods or rules governing behavior; "they have to operate under a system they oppose"; "that language has a complex system for indicating gender" (同)system of rules
a group of physiologically or anatomically related organs or parts; "the body has a system of organs for digestion"
a procedure or process for obtaining an objective; "they had to devise a system that did not depend on cooperation"
the living body considered as made up of interdependent components forming a unified whole; "exercise helped him get the alcohol out of his system"
causing motion or action or change (同)actuating

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2016/09/19 17:39:04」(JST)

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The reticular activating system (RAS), or extrathalamic control modulatory system, is a set of connected nuclei in the brains of vertebrates that is responsible for regulating wakefulness and sleep-wake transitions. As its name implies, its most influential component is the reticular formation.

1 History and etymology
2 Location and structure
- 2.1 Anatomical components
- 2.2 Neurotransmitters
  - 2.2.1 Cholinergic
  - 2.2.2 Adrenergic
3 Function
- 3.1 Regulating sleep-wake transitions
- 3.2 Attention
4 Clinical relevance
- 4.1 Pain
- 4.2 Developmental influences
- 4.3 Pathologies
5 References

History and etymology

Moruzzi and Magoun first investigated the neural components regulating the brain’s sleep-wake mechanisms in 1949. Physiologists had proposed that some structure deep within the brain controlled mental wakefulness and alertness.^[1] It had been thought that wakefulness depended only on the direct reception of afferent (sensory) stimuli at the cerebral cortex.

The direct electrical stimulation of the brain could simulate electrocortical relays. Magoun used this principle to demonstrate, on two separate areas of the brainstem of a cat, how to produce wakefulness from sleep. First the ascending somatic and auditory paths; second, a series of “ascending relays from the reticular formation of the lower brain stem through the mesencephalic tegmentum, subthalamus and hypothalamus to the internal capsule.”^[2] The latter was of particular interest, as this series of relays did not correspond to any known anatomical pathways for the wakefulness signal transduction and was coined the ascending reticular activating system (ARAS).

Next, the significance of this newly identified relay system was evaluated by placing lesions in the medial and lateral portions of the front of the midbrain. Cats with mesancephalic interruptions to the RAS entered into a deep sleep and displayed corresponding brain waves. In alternative fashion, cats with similarly placed interruptions to ascending auditory and somatic pathways exhibited normal sleeping and wakefulness, and could be awakened with somatic stimuli. Because these external stimuli would be blocked by the interruptions, this indicated that the ascending transmission must travel through the newly discovered RAS.

Finally, Magoun recorded potentials within the medial portion of the brain stem and discovered that auditory stimuli directly fired portions of the reticular activating system. Furthermore, single-shock stimulation of the sciatic nerve also activated the medial reticular formation, hypothalamus, and thalamus. Excitation of the RAS did not depend on further signal propagation through the cerebellar circuits, as the same results were obtained following decerebellation and decortication. The researchers proposed that a column of cells surrounding the midbrain reticular formation received input from all the ascending tracts of the brain stem and relayed these afferents to the cortex and therefore regulated wakefulness.^[2]^[3]

Location and structure

Anatomical components

The RAS is composed of several neuronal circuits connecting the brainstem to the cortex. These pathways originate in the upper brainstem reticular core and project through synaptic relays in the rostral intralaminar and thalamic nuclei to the cerebral cortex.^[4] As a result, individuals with bilateral lesions of thalamic intralaminar nuclei are lethargic or somnolent.^[1] Several areas traditionally included in the RAS are:^[5]^[6]

Midbrain Reticular Formation
Mesencephalic Nucleus (in Midbrain)
Thalamic Intralaminar nucleus (centromedian nucleus)
Dorsal Hypothalamus
Tegmentum

The RAS consists of evolutionarily ancient areas of the brain, which are crucial to survival and protected during adverse periods. As a result, the RAS still functions during inhibitory periods of hypnosis.^[7]

Neurotransmitters

The neuronal circuits of the RAS are modulated by complex interactions between a few main neurotransmitters. The RAS contains both cholinergic and adrenergic components, which exhibit synergistic as well as competitive actions to regulate thalamocortical activity and the corresponding behavioral state.

Cholinergic

Shute and Lewis first revealed the presence of a cholinergic component of the RAS,^[8] composed of two ascending mesopontine tegmental pathways rostrally situated between the mesencephalon and the centrum semiovale (semioval center).^[5] These pathways involve cholinergic neurons of the posterior midbrain, the pedunculopontine nucleus (PPN) and the laterodorsal tegmental nucleus (LDT), which are active during waking and REM sleep.^[9] Cholinergic activity is highest when in an awake state and during REM sleep, and is minimal in non-REM sleep^[10] Cholinergic projections descend throughout the reticular formation and ascend to the substantia nigra, basal forebrain, thalamus, and cerebellum;^[11] cholinergic activation in the RAS results in increased acetylcholine release in these areas. Glutamate has also been suggested to play an important role in determining the firing patterns of the tegmental cholinergic neurons.^[12]

It has been recently reported that significant portions of posterior PPN cells are electrically coupled. It appears that this process may help coordinate and enhance rhythmic firing across large populations of cells. This unifying activity may help facilitate signal propagation throughout the RAS and promote sleep-wake transitions. It is estimated that 10 to 15% of RAS cells may be electrically coupled.^[9]

Adrenergic

The adrenergic component of the reticular activating system is closely associated with the noradrenergic neurons of the locus coeruleus. In addition to noradrenergic projections that parallel the aforementioned cholinergic paths, there are ascending projections directly to the cerebral cortex and descending projections to the spinal cord.^[11] Unlike cholinergic neurons, the adrenergic neurons are active during waking and slow wave sleep but cease firing during REM sleep.^[12] In addition, adrenergic neurotransmitters are destroyed much more slowly than acetylcholine. This sustained activity may account for some of the time latency during changes of consciousness.^[5]

More recent work has indicated that the neuronal messenger nitric oxide (NO) may also play an important role in modulating the activity of the noradrenergic neurons in the RAS. NO diffusion from dendrites regulates regional blood flow in the thalamus, where NO concentrations are high during waking and REM sleep and significantly lower during slow-wave sleep. Furthermore, injections of NO inhibitors have been found to affect the sleep-wake cycle and arousal.^[12]

Additionally, it appears that hypocretin/orexin neurons of the hypothalamus activate both the adrenergic and cholinergic components of the RAS and may coordinate activity of the entire system.^[13]

Function

Regulating sleep-wake transitions

The main function of the RAS is to modify and potentiate thalamic and cortical function such that electroencephalogram (EEG) desynchronization ensues.^[1]^[14] There are distinct differences in the brain’s electrical activity during periods of wakefulness and sleep: Low voltage fast burst brain waves (EEG desynchronization) are associated with wakefulness and REM sleep (which are electrophysiologically identical); high voltage slow waves are found during non-REM sleep. Generally speaking, when thalamic relay neurons are in burst mode the EEG is synchronized and when they are in tonic mode it is desynchronized.^[14] Stimulation of the RAS produces EEG desynchronization by suppressing slow cortical waves (0.3–1 Hz), delta waves (1–4 Hz), and spindle wave oscillations (11–14 Hz) and by promoting gamma band (20 – 40 Hz) oscillations.^[13]

The physiological change from a state of deep sleep to wakefulness is reversible and mediated by the RAS.^[3] Inhibitory influence from the brain is active at sleep onset, likely coming from the preoptic area (POA) of the hypothalamus. During sleep, neurons in the RAS will have a much lower firing rate; conversely, they will have a higher activity level during the waking state.^[15] Therefore, low frequency inputs (during sleep) from the RAS to the POA neurons result in an excitatory influence and higher activity levels (awake) will have inhibitory influence. In order that the brain may sleep, there must be a reduction in ascending afferent activity reaching the cortex by suppression of the RAS.^[3]

Attention

The reticular activating system also helps mediate transitions from relaxed wakefulness to periods of high attention.^[6] There is increased regional blood flow (presumably indicating an increased measure of neuronal activity) in the midbrain reticular formation (MRF) and thalamic intralaminar nuclei during tasks requiring increased alertness and attention.

Clinical relevance

Pain

Direct electrical stimulation of the reticular activating system produces pain responses in cats and educes verbal reports of pain in humans.^{[citation needed]} Additionally, ascending reticular activation in cats can produce mydriasis,^{[citation needed]} which can result from prolonged pain. These results suggest some relationship between RAS circuits and physiological pain pathways.^[16]

Developmental influences

There are several potential factors that may adversely influence the development of the reticular activating system:

Preterm birth^[17]

Regardless of birth weight or weeks of gestation, premature birth induces persistent deleterious effects on pre-attentional (arousal and sleep-wake abnormalities), attentional (reaction time and sensory gating), and cortical mechanisms throughout development.

Smoking during pregnancy^[18]

Prenatal exposure to cigarette smoke is known to produce lasting arousal, attentional and cognitive deficits in humans. This exposure can induce up-regulation of nicotinic receptors on α4b2 subunit on Pedunculopontine nucleus (PPN) cells, resulting in increased tonic activity, resting membrane potential, and hyperpolarization-activated cation current. These major disturbances of the intrinsic membrane properties of PPN neurons result in increased levels of arousal and sensory gating deficits (demonstrated by a diminished amount of habituation to repeated auditory stimuli). It is hypothesized that these physiological changes may intensify attentional dysregulation later in life.

Pathologies

Given the importance of the RAS for modulating cortical changes, disorders of the RAS should result in alterations of sleep-wake cycles and disturbances in arousal.^[11] Some pathologies of the RAS may be attributed to age, as there appears to be a general decline in reactivity of the RAS with advancing years.^[19] Changes in electrical coupling have been suggested to account for some changes in RAS activity: If coupling were down-regulated, there would be a corresponding decrease in higher-frequency synchronization (gamma band). Conversely, up-regulated electrical coupling would increase synchronization of fast rhythms that could lead to increased arousal and REM sleep drive.^[9] Specifically, disruption of the RAS has been implicated in the following disorders:

Schizophrenia

Intractable schizophrenic patients have a significant increase (> 60%) in the number of PPN neurons^[11] and dysfunction of NO signaling involved in modulating cholinergic output of the RAS.^[12]

Post-traumatic stress disorder, Parkinson's disease, REM behavior disorder

Patients with these syndromes exhibit a significant (>50%) decrease in the number of locus coeruleus (LC) neurons, resulting is increased disinhibition of the PPN.^[11]

Narcolepsy

Lesions along the PPT/LDT nuclei are associated with narcolepsy.^[20] There is a significant down-regulation of PPN output and a loss of orexin peptides, promoting the excessive daytime sleepiness that is characteristic of this disorder.^[13]

Progressive supranuclear palsy (PSP)

Dysfunction of NO signaling has been implicated in the development of PSP.^[12]

Depression, autism, Alzheimer's disease, attention deficit disorder

The exact role of the RAS in each of these disorders has not yet been identified. However, it is expected that in any neurological or psychiatric disease that manifests disturbances in arousal and sleep-wake cycle regulation, there will be a corresponding dysregulation of some elements of the RAS.^[11]

Parkinson's disease

REM sleep disturbances are common in Parkinson's. It is mainly a dopaminergic disease, but cholinergic nuclei are depleted as well. Degeneration in the RAS begins early in the disease process.^[20]

References

^ ^a ^b ^c Steriade, M. (1996). "Arousal: Revisiting the reticular activating system". Science. 272 (5259): 225–226. doi:10.1126/science.272.5259.225. PMID 8602506.
^ ^a ^b Magoun, H. W. (1952). "AN ASCENDING RETICULAR ACTIVATING SYSTEM IN THE BRAIN STEM". Ama Archives of Neurology and Psychiatry. 67 (2): 145–154. doi:10.1001/archneurpsyc.1952.02320140013002. PMID 14893989.
^ ^a ^b ^c Evans, B.M. (2003). "Sleep, consciousness and the spontaneous and evoked electrical activity of the brain. Is there a cortical integrating mechanism?". Neuophysiologie clinique. 33: 1–10. doi:10.1016/s0987-7053(03)00002-9.
^ Steriade, M (1995). "NEUROMODULATORY SYSTEMS OF THALAMUS AND NEOCORTEX". Seminars in the Neurosciences. 7 (5): 361–370. doi:10.1006/smns.1995.0039.
^ ^a ^b ^c Rothballer, A. B. (1956). "STUDIES ON THE ADRENALINE-SENSITIVE COMPONENT OF THE RETICULAR ACTIVATING SYSTEM". Electroencephalography and Clinical Neurophysiology. 8 (4): 603–621. doi:10.1016/0013-4694(56)90084-0. PMID 13375499.
^ ^a ^b Kinomura, S., Larsson, J., Gulyas, B., & Roland, P. E. (1996). "Activation by attention of the human reticular formation and thalamic intralaminar nuclei". Science. 271 (5248): 512–515. doi:10.1126/science.271.5248.512. PMID 8560267.
^ Svorad, D. (1957). "RETICULAR ACTIVATING SYSTEM OF BRAIN STEM AND ANIMAL HYPNOSIS". Science. 125 (3239): 156–156. doi:10.1126/science.125.3239.156. PMID 13390978.
^ Shute CC, Lewis PR (1967). "The ascending cholinergic reticular system: neocortical, olfactory and subcortical projections". Brain. 90 (3): 497–520. doi:10.1093/brain/90.3.497. PMID 6058140.
^ ^a ^b ^c Garcia-Rill E, Heister DS, Ye M, Charlesworth A, Hayar A (2007). "Electrical coupling: novel mechanism for sleep-wake control". Sleep. 30 (11): 1405–1414. PMC 2082101. PMID 18041475.
^ http://sleepdisorders.sleepfoundation.org/chapter-1-normal-sleep/neurobiology-of-sleep/
^ ^a ^b ^c ^d ^e ^f GarciaRill, E. (1997). "Disorders of the reticular activating system". Medical Hypotheses. 49 (5): 379–387. doi:10.1016/S0306-9877(97)90083-9. PMID 9421802.
^ ^a ^b ^c ^d ^e Vincent, S. R. (2000). "The ascending reticular activating system - from aminergic neurons to nitric oxide". Journal of Chemical Neuroanatomy. 18 (1-2): 23–30. doi:10.1016/S0891-0618(99)00048-4. PMID 10708916.
^ ^a ^b ^c Burlet, S., Tyler, C. J., & Leonard, C. S. (2002). "Direct and indirect excitation of laterodorsal tegmental neurons by hypocretin/orexin peptides: Implications for wakefulness and narcolepsy". Journal of Neuroscience. 22 (7): 2862–2872. PMID 11923451.
^ ^a ^b Reiner, P. B. (1995). "ARE MESOPONTINE CHOLINERGIC NEURONS EITHER NECESSARY OR SUFFICIENT COMPONENTS OF THE ASCENDING RETICULAR ACTIVATING SYSTEM". Seminars in the Neurosciences. 7 (5): 355–359. doi:10.1006/smns.1995.0038.
^ Kumar, V. M., Mallick, B. N., Chhina, G. S., & Singh, B. (1984). "INFLUENCE OF ASCENDING RETICULAR ACTIVATING SYSTEM ON PREOPTIC NEURONAL-ACTIVITY". Experimental Neurology. 86 (1): 40–52. doi:10.1016/0014-4886(84)90065-7. PMID 6479280.
^ Ruth, R. E., & Rosenfeld, J. P. (1977). "TONIC RETICULAR ACTIVATING SYSTEM - RELATIONSHIP TO AVERSIVE BRAIN-STIMULATION EFFECTS". Experimental Neurology. 57 (1): 41–56. doi:10.1016/0014-4886(77)90043-7. PMID 196879.
^ Hall, R. W., Huitt, T. W., Thapa, R., Williams, D., K., Anand, K.J.S., Garcia-Rill, E. (2008). "Long-term deficits of preterm birth: Evidence for arousal and attentional disturbances". Clinical Neurophysiology. 119 (6): 1281–1291. doi:10.1016/j.clinph.2007.12.021. PMC 2670248. PMID 18372212.
^ Garcia-Rill, E., Buchanan, R., McKeon, K., Skinner, R.R., Wallace, T. (2007). "Smoking during pregnancy: Postnatal effects on arousal and attentional brain systems". NeuroToxicology. 28 (5): 915–923. doi:10.1016/j.neuro.2007.01.007. PMC 3320145. PMID 17368773.
^ Robinson, D. (1999). "The technical, neurological and psychological significance of `alpha', `delta' and `theta' waves confounded in EEG evoked potentials: a study of peak latencies". Clinical Neurophysiology. 110 (8): 1427–1434. doi:10.1016/S1388-2457(99)00078-4. PMID 10454278.
^ ^a ^b Schwartz JR, Roth T (December 2008). "Neurophysiology of sleep and wakefulness: basic science and clinical implications". Curr Neuropharmacol. 6: 367–78. doi:10.2174/157015908787386050. PMC 2701283. PMID 19587857.

UpToDate Contents

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5. Surgical resection of sporadic pancreatic neuroendocrine tumors

English Journal

Electrical modulation of neuronal networks in brain-injured patients with disorders of consciousness: A systematic review.

Lemaire JJ1, Sontheimer A2, Nezzar H3, Pontier B4, Luauté J5, Roche B6, Gillart T7, Gabrillargues J8, Rosenberg S9, Sarret C10, Feschet F6, Vassal F11, Fontaine D12, Coste J2.Author information 1IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de neurochirurgie, hôpital Gabriel-Montpied, CHU Clermont-Ferrand, 58, rue Montalembert, 63003 Clermont-Ferrand, France. Electronic address: jjlemaire@chu-clermontferrand.fr.2IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de neurochirurgie, hôpital Gabriel-Montpied, CHU Clermont-Ferrand, 58, rue Montalembert, 63003 Clermont-Ferrand, France.3IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service d'ophtalmologie, hôpital Gabriel-Montpied, CHU Clermont-Ferrand, 58, rue Montalembert, 63003 Clermont-Ferrand, France.4IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de médecine physique et de réadaptation, hôpital Gabriel-Montpied, CHU de Clermont-Ferrand, 58, rue Montalembert, 63003 Clermont-Ferrand, France.5Service de médecine physique et de réadaptation, hospices civils de Lyon, 3, quai des Célestins, BP 2251, 69229 Lyon cedex 02, France.6IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France.7IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de réanimation médico-chirurgicale, hôpital Gabriel-Montpied, 58, rue Montalembert, 63003 Clermont-Ferrand, France.8IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Unité de neuroradiologie, hôpital Gabriel-Montpied, 58, rue Montalembert, 63003 Clermont-Ferrand, France.9IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Unité d'électroencéphalographie et d'exploration fonctionnelle en neurologie, hôpital Gabriel-Montpied, 58, rue Montalembert, 63003 Clermont-Ferrand, France.10IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de neuropédiatrie, hôpital Gabriel-Montpied, CHU de Clermont-Ferrand, 58 rue Montalembert, 63003 Clermont-Ferrand, France.11IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de neurochirurgie, CHU de Saint-Étienne, 42055 Saint-Étienne, France.12IGCNC - EA 728, Image-Guided Clinical Neuroscience and Connectomics, université d'Auvergne, Clermont université, hôpital Gabriel Montpied, 2(e) étage, HC; 58, rue Montalembert, 63003 Clermont-Ferrand, France; Service de neurochirurgie, CHU de Nice, 06006 Nice cedex 1, France.AbstractSix clinical studies of chronic electrical modulation of deep brain circuits published between 1968 and 2010 have reported effects in 55 vegetative or minimally conscious patients. The rationale stimulation was to activate the cortex through the reticular-thalamic complex, comprising the tegmental ascending reticular activating system and its thalamic targets. The most frequent intended target was the central intralaminar zone and adjacent nuclei. Hassler et al. also proposed to modulate the pallidum as part of the arousal and wakefulness system. Stimulation frequency varied from 8Hz to 250Hz. Most patients improved, although in a limited way. Schiff et al. found correlations between central thalamus stimulation and arousal and conscious behaviours. Other treatments that have offered some clinical benefit include drugs, repetitive magnetic transcranial stimulation, median nerve stimulation, stimulation of dorsal column of the upper cervical spinal cord, and stimulation of the fronto-parietal cortex. No one treatment has emerged as a gold standard for practice, which is why clinical trials are still on-going. Further clinical studies are needed to decipher the altered dynamics of neuronal network circuits in patients suffering from severe disorders of consciousness as a step towards novel therapeutic strategies.
Annales francaises d'anesthesie et de reanimation.Ann Fr Anesth Reanim.2013 Dec 19. pii: S0750-7658(13)01218-5. doi: 10.1016/j.annfar.2013.11.007. [Epub ahead of print]
Six clinical studies of chronic electrical modulation of deep brain circuits published between 1968 and 2010 have reported effects in 55 vegetative or minimally conscious patients. The rationale stimulation was to activate the cortex through the reticular-thalamic complex, comprising the tegmental a
PMID 24361283

Gamma band activity in the RAS-intracellular mechanisms.

Garcia-Rill E, Kezunovic N, D'Onofrio S, Luster B, Hyde J, Bisagno V, Urbano FJ.Author information Department of Neurobiology and Developmental Sciences, Center for Translational Neuroscience, University of Arkansas for Medical Sciences, Slot 847, 4301 West Markham St., Little Rock, AR, 72205, USA, GarciaRillEdgar@uams.edu.AbstractGamma band activity participates in sensory perception, problem solving, and memory. This review considers recent evidence showing that cells in the reticular activating system (RAS) exhibit gamma band activity, and describes the intrinsic membrane properties behind such manifestation. Specifically, we discuss how cells in the mesopontine pedunculopontine nucleus, intralaminar parafascicular nucleus, and pontine SubCoeruleus nucleus dorsalis all fire in the gamma band range when maximally activated, but no higher. The mechanisms involve high-threshold, voltage-dependent P/Q-type calcium channels, or sodium-dependent subthreshold oscillations. Rather than participating in the temporal binding of sensory events as in the cortex, gamma band activity in the RAS may participate in the processes of preconscious awareness and provide the essential stream of information for the formulation of many of our actions. We address three necessary next steps resulting from these discoveries: an intracellular mechanism responsible for maintaining gamma band activity based on persistent G-protein activation, separate intracellular pathways that differentiate between gamma band activity during waking versus during REM sleep, and an intracellular mechanism responsible for the dysregulation in gamma band activity in schizophrenia. These findings open several promising research avenues that have not been thoroughly explored. What are the effects of sleep or REM sleep deprivation on these RAS mechanisms? Are these mechanisms involved in memory processing during waking and/or during REM sleep? Does gamma band processing differ during waking versus REM sleep after sleep or REM sleep deprivation?
Experimental brain research. Experimentelle Hirnforschung. Experimentation cerebrale.Exp Brain Res.2013 Dec 6. [Epub ahead of print]
Gamma band activity participates in sensory perception, problem solving, and memory. This review considers recent evidence showing that cells in the reticular activating system (RAS) exhibit gamma band activity, and describes the intrinsic membrane properties behind such manifestation. Specifically,
PMID 24309750

Japanese Journal

脳内局所病変および変性疾患における複雑幻視 (特集器質性(症状性)精神障害の臨床)

西尾慶之,平山和美,内山信 [他]
精神科 14(5), 393-398, 2009-05
NAID 40016599533

「自覚症しらべ」による連続夜勤時の疲労感の表出パターンの検討

久保智英,城憲秀,武山英麿,榎原毅,井上辰樹,高西敏正,荒薦優子,村崎元五,井谷徹
産業衛生学雑誌 50(5), 133-144, 2008-09-20
本研究の目的は,「自覚症しらべ」を用いて連続夜勤時の特徴的な疲労感の変動パターンを明らかにする事であった.10名の健常男性(平均年齢±SD;22.9±3.2歳)が本実験に参加した.参加者は9日間連続して実験室に宿泊し,以下の条件を経験した;適応夜(0:00-7:00),模擬日勤(10:00-18:00),基準夜(0:00-7:00),4連続模擬夜勤(22:00-9:00)および昼間睡眠(12:00 …
NAID 110006951749

Related Pictures

★リンクテーブル★

リンク元	「RAS」「網様体賦活系」
関連記事	「system」「reticula」

「RAS」

Reticular activating system
	Deep dissection of brain-stem. Ventral view. (Reticular formation labeled near center.)
Identifiers
NeuroNames	ancil-231
	Anatomical terms of neuroanatomy [edit on Wikidata]