摘要 There were two stages in the history of the studies on ascending reticular activating system of the brain (ARAS). The first stage began with the ARAS discovery by Magoun and Moruzzi and the following investigations using the methods of stimulation and lesion at that time mainly in acute cats. These studies led to the hypothesis of a "diffuse" and "unspecific" ARAS of the brain stem. The second stage was associated with using more precise neurophysiological and histochemical methods mainly in chronically operated free-moving cats and rats. By 2010, the idea of the ARAS as an organized hierarchy of the cerebral "waking centers" distributed along the entire cerebral axis and releasing all the known neuromediators of low molecular weight together with the most important neuropeptides was formulated. To date, the aforementioned hypothesis has been revised again. The glutamatergic activating system has been discovered and described in detail. Presumably, this system is responsible for the appearance of electroencephalogram (EEG) arousal reaction and maintenance of the neocortex in the state of tonic depolarization during wakefulness and rapid eye movement (REM) sleep. Its destruction results in a deep comatose-like state. At the same time, the activity of all other "waking centers" is probably the result of the cortical activation.
Abstract: There were two stages in the history of the studies on ascending reticular activating system of the brain (ARAS). The first stage began with the ARAS discovery by Magoun and Moruzzi and the following investigations using the methods of stimulation and lesion at that time mainly in acute cats. These studies led to the hypothesis of a "diffuse" and "unspecific" ARAS of the brain stem. The second stage was associated with using more precise neurophysiological and histochemical methods mainly in chronically operated free-moving cats and rats. By 2010, the idea of the ARAS as an organized hierarchy of the cerebral "waking centers" distributed along the entire cerebral axis and releasing all the known neuromediators of low molecular weight together with the most important neuropeptides was formulated. To date, the aforementioned hypothesis has been revised again. The glutamatergic activating system has been discovered and described in detail. Presumably, this system is responsible for the appearance of electroencephalogram (EEG) arousal reaction and maintenance of the neocortex in the state of tonic depolarization during wakefulness and rapid eye movement (REM) sleep. Its destruction results in a deep comatose-like state. At the same time, the activity of all other "waking centers" is probably the result of the cortical activation.
通讯作者:
Vladimir M.Kovalzon,E-mail:kovalzon@sevin.ru
E-mail: kovalzon@sevin.ru
引用本文:
Vladimir M. Kovalzon. Ascending reticular activating system of the brain[J]. 临床转化神经科学, 2016, 2(4): 275-285.
Vladimir M. Kovalzon. Ascending reticular activating system of the brain. Translational Neuroscience and Clinics, 2016, 2(4): 275-285.
20170308103112 Figure 1 Sleep-wake regulation. (a) Wake: The brain stem arousal nuclei (pink) containing ACh, DA, 5-HT, or NA activate the thalamus, hypothalamus, spinal cord motor neurons, and the basal forebrain, and inhibit the VLPA (GABA, galanin); the hypothalamic arousal centers [pink: HA; dark purple: Hcrt] activate the cortex and arousal-related regions in the basal forebrain and brain stem; the thalamus activates the cortex. The glutamatergic MPB in the dorsal pontine tegmentum regulates arousal[28]. (b) NREM sleep: The hypothalamic preoptic area nuclei (dark blue), containing GABA and galanin, inhibit the brain stem and hypothalamic arousal nuclei; the endogenous sleep regulatory substances [adenosine and NO] inhibit basal forebrain arousal nuclei, hypocretin neurons, and TMN neurons; and adenosine activates VLPO neurons. NREM–REM switch: During NREM sleep, serotonergic DR and noradrenergic LC neurons inhibit LDT/PPT neurons. During NREM sleep, vlPAG/LPT neurons inhibit SLD/PC neurons. The GABAergic PZ in the pontomedullary junction promotes sleep[36]. (c) REM sleep: The REM-active brain stem nuclei, including LDT/PPT/SLD/PC and containing ACh, Glu, or GABA, promote activity in the basal forebrain and cortex and induce muscle atonia and rapid eye movements; hypothalamic neurons, containing MCH, promote REM sleep by suppressing REM-inhibitory brain centers, including vlPAG/LPT/DR/LC. NREM–REM switch: During REM sleep, DR/LC neurons become silent, enabling the cholinergic LDT/PPT neurons to generate the hallmarks of REM sleep, including rapid eye movements, EEG activation, and muscle atonia. This reciprocal activity between REM-on (LDT/PPT) and REM-off (DR/LC) neurons drives the cycling between REM and NREM sleep episodes. Additionally, GABAergic neurons participate in the mutual inhibition of REM-activating and REM-suppressing neurons. During REM sleep, SLD/PC neurons use ascending and descending projections to activate the cortex and promote muscle atonia.
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2016, Vol. 2 
