Neuronal activity specific to REM sleep and its relationship to breathing

Netick, Allan; Orem, John; Dement, William C.

doi:10.1016/0006-8993(77)90900-3

Cited by 102 publications

(20 citation statements)

References 9 publications

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“…To date, most cells tonically activated during REMS have been recorded from relatively more rostral and more medial regions of the medullary reticular formation in cats [31], [32], [33], [34], [35]. A recent study in chronically instrumented, REMS-deprived and head-restrained rats found that the population of REMS-on medullary reticular neurons extends further caudal and lateral than in earlier reports [40].…”

Section: Discussionmentioning

confidence: 94%

“…This is due, in part, to historically greater attention paid to the pontine mechanisms but the progress is also hampered by the technical difficulty to record cell activities across the sleep-wake cycle at sites located close to the highly mobile spino-medullary junction. Nevertheless, cell recordings in chronically instrumented cats demonstrated that the medial reticular formation of the rostral medulla contains appreciable numbers of REMS-on neurons [31], [32], [33], [34], [35] and that serotonergic cells located along the medullary midline have REMS-off firing patterns [36], [37], [38]. However, the studies in chronically instrumented, behaving animals are limited in that the locations of the recording sites often cannot be precisely determined and the neurochemical identity of the recorded neurons is difficult to ascertain.…”

Section: Introductionmentioning

confidence: 99%

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Evidence That Adrenergic Ventrolateral Medullary Cells Are Activated whereas Precerebellar Lateral Reticular Nucleus Neurons Are Suppressed during REM Sleep

et al. 2013

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Rapid eye movement sleep (REMS) is generated in the brainstem by a distributed network of neurochemically distinct neurons. In the pons, the main subtypes are cholinergic and glutamatergic REMS-on cells and aminergic REMS-off cells. Pontine REMS-on cells send axons to the ventrolateral medulla (VLM), but little is known about REMS-related activity of VLM cells. In urethane-anesthetized rats, dorsomedial pontine injections of carbachol trigger REMS-like episodes that include cortical and hippocampal activation and suppression of motoneuronal activity; the episodes last 4–8 min and can be elicited repeatedly. We used this model to determine whether VLM catecholaminergic cells are silenced during REMS, as is typical of most aminergic neurons studied to date, and to investigate other REMS-related cells in this region. In 18 anesthetized, paralyzed and artificially ventilated rats, we obtained extracellular recordings from VLM cells when REMS-like episodes were elicited by pontine carbachol injections (10 mM, 10 nl). One major group were the cells that were activated during the episodes (n = 10). Their baseline firing rate of 3.7±2.1 (SD) Hz increased to 9.7±2.1 Hz. Most were found in the adrenergic C1 region and at sites located less than 50 µm from dopamine β-hydroxylase-positive (DBH+) neurons. Another major group were the silenced or suppressed cells (n = 35). Most were localized in the lateral reticular nucleus (LRN) and distantly from any DBH+ cells. Their baseline firing rates were 6.8±4.4 Hz and 15.8±7.1 Hz, respectively, with the activity of the latter reduced to 7.4±3.8 Hz. We conclude that, in contrast to the pontine noradrenergic cells that are silenced during REMS, medullary adrenergic C1 neurons, many of which drive the sympathetic output, are activated. Our data also show that afferent input transmitted to the cerebellum through the LRN is attenuated during REMS. This may distort the spatial representation of body position during REMS.

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Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

Evidence That Adrenergic Ventrolateral Medullary Cells Are Activated whereas Precerebellar Lateral Reticular Nucleus Neurons Are Suppressed during REM Sleep

et al. 2013

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“…In adult cats, classes of medullary neurons have been identified that discharge during wakefulness, during REM sleep [35,36,37], and during REM sleep as well as waking movements [35,38,39]. Medullary neurons with similar discharge profiles have also been identified in adults rats [40,41].…”

Section: Discussionmentioning

confidence: 99%

The Neural Substrates of Infant Sleep in Rats

et al. 2005

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Sleep is a poorly understood behavior that predominates during infancy but is studied almost exclusively in adults. One perceived impediment to investigations of sleep early in ontogeny is the absence of state-dependent neocortical activity. Nonetheless, in infant rats, sleep is reliably characterized by the presence of tonic (i.e., muscle atonia) and phasic (i.e., myoclonic twitching) components; the neural circuitry underlying these components, however, is unknown. Recently, we described a medullary inhibitory area (MIA) in week-old rats that is necessary but not sufficient for the normal expression of atonia. Here we report that the infant MIA receives projections from areas containing neurons that exhibit state-dependent activity. Specifically, neurons within these areas, including the subcoeruleus (SubLC), pontis oralis (PO), and dorsolateral pontine tegmentum (DLPT), exhibit discharge profiles that suggest causal roles in the modulation of muscle tone and the production of myoclonic twitches. Indeed, lesions in the SubLC and PO decreased the expression of muscle atonia without affecting twitching (resulting in “REM sleep without atonia”), whereas lesions of the DLPT increased the expression of atonia while decreasing the amount of twitching. Thus, the neural substrates of infant sleep are strikingly similar to those of adults, a surprising finding in light of theories that discount the contribution of supraspinal neural elements to sleep before the onset of state-dependent neocortical activity.

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“…In contrast, controls showed an increased frequency of obstructive apneas, predominantly caused by airway pathologies, allergic rhinitis being the most common (6/24). The increased frequency of sleep disorder in CM II patients, may be explained by the variable degree of brain stem abnormalities in CM II patients 21,22 , generally involving midbrain, pons and medulla oblongata, where are localized neurons of the respiratory regulation, and neurons of the REM sleep and of the movement control during sleep [23][24][25] . Analyzing these data, it is possible to conclude that sleep disorders are more prone to cause attention deficit than the presence of CM II alone, since in CM II patients without sleep disorders no attention deficit could be detected (Table 4).…”

Section: Discussionmentioning

confidence: 99%

Sleep disorder: a possible cause of attention deficit in children and adolescents with Chiari malformation type II

Filho¹,

Pratesi²

2009

Arq. Neuro-Psiquiatr.

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-Background: Attention deficit may be related to sleep disorders in Chiari malformation type II (CMII). Our aim is identify sleep disorders and their specific contribution in attention deficit. Method: We selected 24 patients with CM II and 24 without CM II. DSM-IV criteria and a neuropsychological analysis were applied in all. All patients underwent full night polysomnography. Results: 14 CM II patients presented sleep apnea syndrome, REM sleep behavior disorder and periodic limb movement in sleep; six patients without CM II presented sleep apnea syndrome. Among these patients, 12 (six with CM II and six without CM II) presented attention deficit related to the sleep disorders. Conclusion: Sleep disorders may impair cognitive functions, as attention, and contribute to poor quality of learning also in patients with CM II.KEy WORDS: polysomnography, REM sleep behavior disorder, apnea, cognition, attention deficit disorder. Distúrbios do sono: possível causa de déficit de atenção em crianças e adolescentes com malformação de Chiari tipo IIResumo -Introdução: Déficits de atenção podem estar relacionados a distúrbios do sono em indivíduos com malformação de Chiari tipo II (CM II). Nosso objetivo é identificar distúrbios do sono e sua contribuição para a ocorrência de déficit de atenção. Método: Foram selecionados 24 pacientes com CM II e 24 sem CM II. Todos foram submetidos à avaliação neuropsicológica, aos critérios do DSM-IV e a polissonografia. Resultados: 14 pacientes com CM II apresentaram síndrome da apnéia do sono, distúrbio do comportamento da fase do sono REM e movimentos periódicos dos membros em sono; seis pacientes sem CM II apresentaram síndrome da apnéia do sono. Entre estes pacientes, 12 (seis com CM II e seis sem CM II) apresentaram déficit de atenção relacionado a distúrbios do sono. Conclusão: Distúrbios do sono podem prejudicar funções cognitivas, como a atenção, contribuindo para a piora da qualidade de aprendizado também em pacientes com CM II.PAlAVRAS-ChAVE: polissonografia, distúrbio do comportamento da fase do sono com movimentos oculares rápidos, apnéia, cognição, transtorno do déficit de atenção. The central nervous system (CNS) abnormality characterized by herniation of cerebellar tonsils below the plane of foramen magnum was initially described by Chiari in 1891. Subsequently, the same author expanded the spectrum of abnormalities of the craniocervical junction including disorders that are currently recognized as Chiari malformation (CM) type I, II, III and IV. These congenital disorders disclose complex physical and neuropsychological symptomatology and are associated with developmental anomalies of both the spine and brain 1 . The CM type II (CM II) is characterized by the descent of the inferior vermis and cerebellar hemispheres through the foramen magnum with a displacement of the brain stem (medulla, fourth ventricle, and lower portion of the pons) inside the spinal canal, resulting in aqueduct and fourth ventricle elongation 1,2 . Myelomeningocele is present in almost all c...

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Neuronal activity specific to REM sleep and its relationship to breathing

Cited by 102 publications

References 9 publications

Evidence That Adrenergic Ventrolateral Medullary Cells Are Activated whereas Precerebellar Lateral Reticular Nucleus Neurons Are Suppressed during REM Sleep

Evidence That Adrenergic Ventrolateral Medullary Cells Are Activated whereas Precerebellar Lateral Reticular Nucleus Neurons Are Suppressed during REM Sleep

The Neural Substrates of Infant Sleep in Rats

Sleep disorder: a possible cause of attention deficit in children and adolescents with Chiari malformation type II

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