网状结构
参考

↑  Gray, Henry. . Bartleby.com.   [2019-09-12]. （原始内容存档于2018-04-21）.
↑  .   [2024-01-31]. （原始内容存档于2024-01-31）.
1 2 3 4 5 6 7 8 9  Iwańczuk W, Guźniczak P. . Anaesthesiol Intensive Ther. 2015, 47 (2): 162–167. PMID 25940332. doi:10.5603/AIT.2015.0015. The ascending reticular activating system (ARAS) is responsible for a sustained wakefulness state. It receives information from sensory receptors of various modalities, transmitted through spinoreticular pathways and cranial nerves (trigeminal nerve – polymodal pathways, olfactory nerve, optic nerve and vestibulocochlear nerve – monomodal pathways). These pathways reach the thalamus directly or indirectly via the medial column of reticular formation nuclei (magnocellular nuclei and reticular nuclei of pontine tegmentum). The reticular activating system begins in the dorsal part of the posterior midbrain and anterior pons, continues into the diencephalon, and then divides into two parts reaching the thalamus and hypothalamus, which then project into the cerebral cortex (Fig. 1). The thalamic projection is dominated by cholinergic neurons originating from the pedunculopontine tegmental nucleus of pons and midbrain (PPT) and laterodorsal tegmental nucleus of pons and midbrain (LDT) nuclei [17, 18]. The hypothalamic projection involves noradrenergic neurons of the locus coeruleus (LC) and serotoninergic neurons of the dorsal and median raphe nuclei (DR), which pass through the lateral hypothalamus and reach axons of the histaminergic tubero-mamillary nucleus (TMN), together forming a pathway extending into the forebrain, cortex and hippocampus. Cortical arousal also takes advantage of dopaminergic neurons of the substantia nigra (SN), ventral tegmenti area (VTA) and the periaqueductal grey area (PAG). Fewer cholinergic neurons of the pons and midbrain send projections to the forebrain along the ventral pathway, bypassing the thalamus [19, 20].
1 2 3 4 5 6 7 8  Brudzynski SM. . Journal of Molecular Neuroscience. July 2014, 53 (3): 436–445. PMID 24272957. S2CID 14615039. doi:10.1007/s12031-013-0179-1. Understanding of arousing and wakefulness-maintaining functions of the ARAS has been further complicated by neurochemical discoveries of numerous groups of neurons with the ascending pathways originating within the brainstem reticular core, including pontomesencephalic nuclei, which synthesize different transmitters and release them in vast areas of the brain and in the entire neocortex (for review, see Jones 2003; Lin et al. 2011). They included glutamatergic, cholinergic, noradrenergic, dopaminergic, serotonergic, histaminergic, and orexinergic systems (for review, see Lin et al. 2011). ... The ARAS represented diffuse, nonspecific pathways that, working through the midline and intralaminar thalamic nuclei, could change activity of the entire neocortex, and thus, this system was suggested initially as a general arousal system to natural stimuli and the critical system underlying wakefulness (Moruzzi and Magoun 1949; Lindsley et al. 1949; Starzl et al. 1951, see stippled area in Fig. 1). ... It was found in a recent study in the rat that the state of wakefulness is mostly maintained by the ascending glutamatergic projection from the parabrachial nucleus and precoeruleus regions to the basal forebrain and then relayed to the cerebral cortex (Fuller et al. 2011). ... Anatomical studies have shown two main pathways involved in arousal and originating from the areas with cholinergic cell groups, one through the thalamus and the other, traveling ventrally through the hypothalamus and preoptic area, and reciprocally connected with the limbic system (Nauta and Kuypers 1958; Siegel 2004). ... As counted in the cholinergic connections to the thalamic reticular nucleus ...
1 2 3 4 5 6 7 8 9  Schwartz MD, Kilduff TS. . The Psychiatric Clinics of North America. December 2015, 38 (4): 615–644. PMC 4660253 . PMID 26600100. doi:10.1016/j.psc.2015.07.002. This ascending reticular activating system (ARAS) is comprised of cholinergic laterodorsal and pedunculopontine tegmentum (LDT/PPT), noradrenergic locus coeruleus (LC), serotonergic (5-HT) Raphe nuclei and dopaminergic ventral tegmental area (VTA), substantia nigra (SN) and periaqueductal gray projections that stimulate the cortex directly and indirectly via the thalamus, hypothalamus and BF.6, 12-18 These aminergic and catecholaminergic populations have numerous interconnections and parallel projections which likely impart functional redundancy and resilience to the system.6, 13, 19 ... More recently, the medullary parafacial zone (PZ) adjacent to the facial nerve was identified as a sleep-promoting center on the basis of anatomical, electrophysiological and chemo- and optogenetic studies.23, 24 GABAergic PZ neurons inhibit glutamatergic parabrachial (PB) neurons that project to the BF,25 thereby promoting NREM sleep at the expense of wakefulness and REM sleep. ... The Hcrt neurons project widely throughout the brain and spinal cord92, 96, 99, 100 including major projections to wake-promoting cell groups such as the HA cells of the TM,101 the 5-HT cells of the dorsal Raphe nuclei (DRN),101 the noradrenergic cells of the LC,102 and cholinergic cells in the LDT, PPT, and BF.101, 103 ... Hcrt directly excites cellular systems involved in waking and arousal including the LC,102, 106, 107 DRN,108, 109 TM,110-112 LDT,113, 114 cholinergic BF,115 and both dopamine (DA) and non-DA neurons in the VTA.116, 117
1 2 3 4 5 6  Malenka RC, Nestler EJ, Hyman SE.  2nd. New York: McGraw-Hill Medical. 2009: 295. ISBN 978-0071481274. The RAS is a complex structure consisting of several different circuits including the four monoaminergic pathways ... The norepinephrine pathway originates from the locus ceruleus (LC) and related brainstem nuclei; the serotonergic neurons originate from the raphe nuclei within the brainstem as well; the dopaminergic neurons originate in ventral tegmental area (VTA); and the histaminergic pathway originates from neurons in the tuberomammillary nucleus (TMN) of the posterior hypothalamus. As discussed in Chapter 6, these neurons project widely throughout the brain from restricted collections of cell bodies. Norepinephrine, serotonin, dopamine, and histamine have complex modulatory functions and, in general, promote wakefulness. The PT in the brain stem is also an important component of the ARAS. Activity of PT cholinergic neurons (REM-on cells) promotes REM sleep. During waking, REM-on cells are inhibited by a subset of ARAS norepinephrine and serotonin neurons called REM-off cells.
1 2  Squire L.  4th. Amsterdam: Elsevier/Academic Press. 2013: 1095. ISBN 978-0123858702.
1 2 3 4  Saper CB, Fuller PM. . Current Opinion in Neurobiology. June 2017, 44: 186–192. PMC 5531075 . PMID 28577468. doi:10.1016/j.conb.2017.03.021. Parabrachial and pedunculopontine glutamatergic arousal system
Retrograde tracers from the BF have consistently identified one brainstem site of input that is not part of the classical monoaminergic ascending arousal system: glutamatergic neurons in the parabrachial and pedunculopontine nucleus ... Juxtacellular recordings from pedunculopontine neurons have found that nearly all cholinergic neurons in this region, as well as many glutamatergic and GABAergic neurons, are most active during wake and REM sleep [25], although some of the latter neurons were maximally active during either wake or REM, but not both. ... [Parabrachial and pedunculopontine glutamatergic neurons] provide heavy innervation to the lateral hypothalamus, central nucleus of the amygdala, and BF
1 2  Pedersen NP, Ferrari L, Venner A, Wang JL, Abbott SG, Vujovic N, Arrigoni E, Saper CB, Fuller PM. . Nature Communications. November 2017, 8 (1): 1405. Bibcode:2017NatCo...8.1405P. PMC 5680228 . PMID 29123082. doi:10.1038/s41467-017-01004-6. Basic and clinical observations suggest that the caudal hypothalamus comprises a key node of the ascending arousal system, but the cell types underlying this are not fully understood. Here we report that glutamate-releasing neurons of the supramammillary region (SuMvglut2) produce sustained behavioral and EEG arousal when chemogenetically activated.
1 2 3  Burlet S, Tyler CJ, Leonard CS. . J. Neurosci. April 2002, 22 (7): 2862–2872. PMC 6758338 . PMID 11923451. doi:10.1523/JNEUROSCI.22-07-02862.2002.
↑  Malenka RC, Nestler EJ, Hyman SE.  2nd. New York: McGraw-Hill Medical. 2009: 295. ISBN 978-0071481274. Orexin neurons are located in the lateral hypothalamus. They are organized in a widely projecting manner, much like the monoamines (Chapter 6), and innervate all of the components of the ARAS. They excite the REM-off monoaminergic neurons during wakefulness and the PT cholinergic neurons during REM sleep. They are inhibited by the VLPO neurons during NREM sleep.
1 2  Cherasse Y, Urade Y. . International Journal of Molecular Sciences. November 2017, 18 (11): 2334. PMC 5713303 . PMID 29113075. doi:10.3390/ijms18112334 . The regulation of sleep and wakefulness involves many regions and cellular subtypes in the brain. Indeed, the ascending arousal system promotes wakefulness through a network composed of the monaminergic neurons in the locus coeruleus (LC), histaminergic neurons in the tuberomammilary nucleus (TMN), glutamatergic neurons in the parabrachial nucleus (PB) ...
↑  Fuller PM, Fuller P, Sherman D, Pedersen NP, Saper CB, Lu J. . The Journal of Comparative Neurology. April 2011, 519 (5): 933–956. PMC 3119596 . PMID 21280045. doi:10.1002/cne.22559.
1 2  Kinomura S, Larsson J, Gulyás B, Roland PE. . Science. January 1996, 271 (5248): 512–515. Bibcode:1996Sci...271..512K. PMID 8560267. S2CID 43015539. doi:10.1126/science.271.5248.512. This corresponds to the centro-median and centralis lateralis nuclei of the intralaminar group
↑  VandenBos, Gary R (编). . APA dictionary of psychology 2nd (Washington, DC: American Psychological Association). 2015: 57. ISBN 978-1433819445. doi:10.1037/14646-000. a state of motor nonresponsiveness in nonhuman animals, produced by stroking, salient stimuli, or physical restraint. It is called “hypnosis” because of a claimed resemblance to human hypnosis and trance
↑  Svorad D. . Science. January 1957, 125 (3239): 156. Bibcode:1957Sci...125..156S. PMID 13390978. doi:10.1126/science.125.3239.156.
1 2  Jang SH, Kwon HG. . Neurosci. Lett. October 2015, 606: 200–203. PMID 26363340. S2CID 37083435. doi:10.1016/j.neulet.2015.09.004.
↑  Jones, BE. . Annals of the New York Academy of Sciences. 2008, 1129 (1): 26–34. Bibcode:2008NYASA1129...26J. PMID 18591466. S2CID 16682827. doi:10.1196/annals.1417.026.
↑  Purves et al (2018b)，Box 28A – Electroencephalography, pp. 647–649
1 2  Steriade, M. . Science. 1996, 272 (5259): 225–226. Bibcode:1996Sci...272..225S. PMID 8602506. S2CID 39331177. doi:10.1126/science.272.5259.225.
1 2  Reiner, P. B. . Seminars in Neuroscience. 1995, 7 (5): 355–359. S2CID 5575547. doi:10.1006/smns.1995.0038.
1 2 3  Evans, B.M. . Neurophysiologie Clinique. 2003, 33 (1): 1–10. PMID 12711127. S2CID 26159370. doi:10.1016/s0987-7053(03)00002-9.
↑  Purves et al (2018b)
↑  Mohan Kumar V, Mallick BN, Chhina GS, Singh B. . Exp. Neurol. October 1984, 86 (1): 40–52. PMID 6479280. S2CID 28688574. doi:10.1016/0014-4886(84)90065-7.
↑  Tindall SC. https://www.ncbi.nlm.nih.gov/books/NBK380/#A1740 |chapterurl=缺少标题 (帮助). . Butterworth Publishers. 1990  [2008-07-04]. ISBN 978-0409900774. （原始内容存档于2009-01-29）.
↑  Nolte (编).  5th. : 262–290.
1 2  Ruth RE, Rosenfeld JP. . Exp. Neurol. October 1977, 57 (1): 41–56. PMID 196879. S2CID 45019057. doi:10.1016/0014-4886(77)90043-7.
↑  Robinson, D. . Clinical Neurophysiology. 1999, 110 (8): 1427–1434. PMID 10454278. S2CID 38882496. doi:10.1016/S1388-2457(99)00078-4.
↑  Lawrence, Eleanor (编). . Henderson's dictionary of biology 13th (Pearson Education Limited). 2005: 195. ISBN 978-0131273849.
↑  Garcia-Rill E, Heister DS, Ye M, Charlesworth A, Hayar A. . Sleep. 2007, 30 (11): 1405–1414. PMC 2082101 . PMID 18041475. doi:10.1093/sleep/30.11.1405.
1 2  Schwartz JR, Roth T. . Curr Neuropharmacol. December 2008, 6 (4): 367–378. PMC 2701283 . PMID 19587857. doi:10.2174/157015908787386050.
↑  Vincent, S. R. . Journal of Chemical Neuroanatomy. 2000, 18 (1–2): 23–30. PMID 10708916. S2CID 36236217. doi:10.1016/S0891-0618(99)00048-4.
↑  Hall RW, Huitt TW, Thapa R, Williams DK, Anand KJ, Garcia-Rill E. . Clin Neurophysiol. June 2008, 119 (6): 1281–1291. PMC 2670248 . PMID 18372212. doi:10.1016/j.clinph.2007.12.021.
↑  Garcia-Rill E, Buchanan R, McKeon K, Skinner RD, Wallace T. . Neurotoxicology. September 2007, 28 (5): 915–923. PMC 3320145 . PMID 17368773. doi:10.1016/j.neuro.2007.01.007.
1 2 3  Squire L.  4th. Amsterdam: Elsevier/Academic Press. 2013: 631–632. ISBN 978-0123858702.
↑  FitzGerald MT, Gruener G, Mtui E. . Philadelphia: Saunders Elsevier. 2012: 192. ISBN 978-0702037382.
↑  Brownstone, Robert M.; Chopek, Jeremy W. . Frontiers in Neural Circuits. 2018, 12: 30. ISSN 1662-5110. PMC 5915564 . PMID 29720934. doi:10.3389/fncir.2018.00030 .
↑  Pearson, Keir G; Gordon, James E. Kandel , 编.  5th. United States: McGraw-Hill. 2013. The Brain Stem and Cerebellum Integrate Sensory Signals for Posture, p. 954. ISBN 978-0071390118.  Editors list列表中的|first2=缺少|last2= (帮助); Editors list列表中的|first4=缺少|last4= (帮助)
1 2  Michael-Titus et al (2010b)
1 2  Magoun HW. . AMA Arch Neurol Psychiatry. February 1952, 67 (2): 145–154; discussion 167–171. PMID 14893989. doi:10.1001/archneurpsyc.1952.02320140013002.