Discharge correlations between neurons in the nucleus parabrachialis medialis during sleep-waking states

Selected examples from man and canine experiments with time series of reticular neurons, respiration, arterial blood pressure, and cutaneous forehead blood content fluctuations were analyzed using multiscaled Time-Frequency-Distribution (TFD), Post-Event-Scan (PES), and Pointwise Transinformation (PTI), resp.. We found in both experiments a "0.15 Hz rhythm" which exhibited periods of spindle wave epochs (increasing and decreasing amplitudes) to be phase synchronized with respiration at 1:2, 1:1 and 2:1 integer number ratios. At times of these wave-epochs and n:m phase-synchronization, the "0.15 Hz rhythm" appeared also in heart rate and arterial blood pressure fluctuations. If phase synchronization of the "0.15 Hz rhythm" with respiration was established at a 1:1 integer number ratio, it was maintained throughout and resulted in consensualization of all cardio-vascular-respiratory oscillations at 0.15 Hz. Analysis of a canine experiment supplied evidence that the emergence of the "0.15Hz rhythm" and n:m phase synchronization appears to result from a decline in the level of the general activity of the organism which was associated with a decline in the level of activity of reticular neurons in the lower brainstem network. These findings corroborate the notion of the "0.15 Hz rhythm" to be a state marker of the `trophotropic mode of operation` which was introduced by W.R. Hess.

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“…Many authors have observed and described such rhythms in RF neurons using animal experiments (8)(9)(10)(11)(47)(48)(49)(50).…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular rhythms in the 0.15-Hz band: common origin of identical phenomena in man and dog in the reticular formation of the brain stem?

Perlitz

Lambertz

Cotuk

et al. 2004

Pflugers Arch - Eur J Physiol

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“…The central control of respiration is a complex process involving several brainstem areas, each controlling a different aspect of breathing. Using lesion, stimulation, and single cell activity recording techniques, a number of studies have provided strong evidences supporting the altered activity of the PBN neurons associated with REM sleep is the causal factor for respiratory fluctuations during REM sleep (Bertrand and Hugelin, 1971;Cohen, 1971;Harper and Sieck, 1980;Knox and King, 1976;Lydic and Orem, 1979). The most striking cardiovascular changes in REM sleep involve phasically occurring increases in heart rate and blood pressure that coincide with the other phasic events of REM sleep (Baust and Bohnert, 1969;Gassel et al, 1964;Gottesmann, 1969;Mancia and Zanchetti, 1980;Spreng et al, 1968).…”

Section: Fluctuations In Autonomic Systemsmentioning

confidence: 95%

Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Datta

MacLean

2007

Neuroscience & Biobehavioral Reviews

268

249

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At its most basic level, the function of mammalian sleep can be described as a restorative process of the brain and body; recently, however, progressive research has revealed a host of vital functions to which sleep is essential. Although many excellent reviews on sleep behavior have been published, none have incorporated contemporary studies examining the molecular mechanisms that govern the various stages of sleep. Utilizing a holistic approach, this review is focused on the basic mechanisms involved in the transition from wakefulness, initiation of sleep and the subsequent generation of slow-wave sleep and rapid eye movement (REM) sleep. Additionally, using recent molecular studies and experimental evidence that provides a direct link to sleep as a behavior, we have developed a new model, the cellular-molecular-network model, explaining the mechanisms responsible for regulating REM sleep. By analyzing the fundamental neurobiological mechanisms responsible for the generation and maintenance of sleep-wake behavior in mammals, we intend to provide a broader understanding of our present knowledge in the field of sleep research.

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“…Such cells could be premotor cells for upper airway motoneurons, vagal motoneurons, or neurons involved in mediating respiratory modulation of cardiovascular outputs. Respiratory-modulated neurons located in the pontine parabrachial region increased or decreased their firing rates on transition from wakefulness to NREM sleep, with the average change being a small decrease (187,496). It is of note that the pontine parabrachial region gives origin to projections to orofacial motor nuclei (109, 132, 154, 155, 512, 551, 557).…”

Section: Neurochemically Distinct Central Neuronal Systems With Statementioning

confidence: 99%

“…The variability at the neuronal level correlates with the breath-to-breath changes in the magnitude of diaphragmatic activity and tracheal pressure (389), as expected given that many of the studied medullary respiratory neurons were bulbo-spinal neurons sending axons to phrenic motoneurons. Similar to medullary respiratory neurons, many pontine parabrachial respiratory and nonrespiratory neurons increase their activity during REM sleep (187). …”

Section: Neurochemically Distinct Central Neuronal Systems With Statementioning

confidence: 99%

Neural Control of the Upper Airway: Respiratory and State‐Dependent Mechanisms

Kubin

2016

Comprehensive Physiology

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Upper airway muscles subserve many essential for survival orofacial behaviors, including their important role as accessory respiratory muscles. In the face of certain predisposition of craniofacial anatomy, both tonic and phasic inspiratory activation of upper airway muscles is necessary to protect the upper airway against collapse. This protective action is adequate during wakefulness, but fails during sleep which results in recurrent episodes of hypopneas and apneas, a condition known as the obstructive sleep apnea syndrome (OSA). Although OSA is almost exclusively a human disorder, animal models help unveil the basic principles governing the impact of sleep on breathing and upper airway muscle activity. This article discusses the neuroanatomy, neurochemistry, and neurophysiology of the different neuronal systems whose activity changes with sleep-wake states, such as the noradrenergic, serotonergic, cholinergic, orexinergic, histaminergic, GABAergic and glycinergic, and their impact on central respiratory neurons and upper airway motoneurons. Observations of the interactions between sleep-wake states and upper airway muscles in healthy humans and OSA patients are related to findings from animal models with normal upper airway, and various animal models of OSA, including the chronic-intermittent hypoxia model. Using a framework of upper airway motoneurons being under concurrent influence of central respiratory, reflex and state-dependent inputs, different neurotransmitters, and neuropeptides are considered as either causing a sleep-dependent withdrawal of excitation from motoneurons or mediating an active, sleep-related inhibition of motoneurons. Information about the neurochemistry of state-dependent control of upper airway muscles accumulated to date reveals fundamental principles and may help understand and treat OSA.

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Discharge correlations between neurons in the nucleus parabrachialis medialis during sleep-waking states

Cited by 25 publications

References 28 publications

Cardiovascular rhythms in the 0.15-Hz band: common origin of identical phenomena in man and dog in the reticular formation of the brain stem?

Cardiovascular rhythms in the 0.15-Hz band: common origin of identical phenomena in man and dog in the reticular formation of the brain stem?

Neurobiological mechanisms for the regulation of mammalian sleep–wake behavior: Reinterpretation of historical evidence and inclusion of contemporary cellular and molecular evidence

Neural Control of the Upper Airway: Respiratory and State‐Dependent Mechanisms

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