Disinhibition of perifornical hypothalamic neurones activates noradrenergic neurones and blocks pontine carbachol‐induced REM sleep‐like episodes in rats

Lu, Jackie W.; Fenik, Victor B.; Branconi, Jennifer L.; Mann, Graziella L.; Rukhadze, Irma; Kubin, Leszek

doi:10.1113/jphysiol.2007.127613

Cited by 31 publications

(57 citation statements)

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“…As described previously (Kubin and Fenik, 2004;Fenik et al, 2005;Lu et al, 2007), carbacholinduced REMS-like episodes were characterized by activation of the cortical EEG in 6-12 Hz range, the appearance of hippocampal theta-like rhythm (3-4 Hz in anaesthetized rats), decreased respiratory rate and suppression of XII nerve activity. The episodes occurred within 59.7±8.6 s (range: 2.4-390 s) following the onset of carbachol injections, and their mean duration was 4.5±0.4 min (range: 1-13 min).…”

Section: Temporal Distribution and Cumulative Duration Of Rems-like Ementioning

confidence: 82%

Section: Temporal Distribution and Cumulative Duration Of Rems-like Ementioning

confidence: 99%

“…In this model, one can repeatedly elicit REMS-like episodes comprising cortical and hippocampal activation, silencing of brainstem aminergic cells and suppression of motoneuronal activity (Kubin, 2001;Fenik et al, 2002;Kubin and Fenik, 2004). The episodes likely involve cellular and network activity that, albeit simplified, bears major similarities to that during natural REMS in behaving animals (Kubin, 2001;Fenik et al, 2002;Fenik et al, 2005;Lu et al, 2007). We found that Fos expression in SubC and A5 neurons was negatively correlated with the cumulative duration of REMS-like state in accordance with earlier single-cell recording studies showing that these cells cease firing during REMS.…”

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confidence: 99%

“…The injections were placed at the anterior-posterior levels from AP-8.1 to AP-8.9 caudal to bregma (Paxinos and Watson, 1997), within the dorsomedial pontine reticular formation region that we previously determined to be effective in eliciting REMS-like episodes (Kubin, 2001;Fenik et al, 2005;Lu et al, 2007). Figure 1 shows the locations of the centers of all injections superimposed on two closest standard brain sections from a rat brain atlas (Paxinos and Watson, 1997).As described previously (Kubin and Fenik, 2004;Fenik et al, 2005;Lu et al, 2007), carbacholinduced REMS-like episodes were characterized by activation of the cortical EEG in 6-12 Hz range, the appearance of hippocampal theta-like rhythm (3-4 Hz in anaesthetized rats), decreased respiratory rate and suppression of XII nerve activity. The episodes occurred within 59.7±8.6 s (range: 2.4-390 s) following the onset of carbachol injections, and their mean duration was 4.5±0.4 min (range: 1-13 min).…”

mentioning

confidence: 99%

“…Compared to behaving animals, the carbachol-injected anesthetized rat is a simplified model of REMS, but nevertheless it exhibits major hallmarks of this state, including cortical activation, theta-like activity in the hippocampus, silencing of LC and A5 cells and depression of activity in XII motoneurons (Kubin, 2001;Fenik et al, 2002;Kubin and Fenik, 2004;Fenik et al, 2005). In addition, in both chronically instrumented, behaving rats (Alam et al, 2005) and anesthetized rats (Lu et al, 2007), the occurrence of REMS, or REMS-like state, is blocked by activation of neurons located in a well-established wake-promoting region of the posterior hypothalamus. The anesthetized rat carbachol model does not generate phasic events of REMS, such as eye movements, bursts of motoneuronal activity or rapid variations of respiratory rate and arterial blood pressure.…”

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Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats

et al. 2008

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Pontine noradrenergic neurons of the locus coeruleus (LC) and sub-coeruleus (SubC) region cease firing during rapid eye movement sleep (REMS). This plays a permissive role in the generation of REMS and may contribute to state-dependent modulation of transmission in the central nervous system. Whether all pontomedullary catecholaminergic neurons, including those in the A1/C1, A2/ C2 and A7 groups, have REMS-related suppression of activity has not been tested. We used Fos protein expression as an indirect marker of the level of neuronal activity and linear regression analysis to determine whether pontomedullary cells identified by tyrosine hydroxylase (TH) immunohistochemistry have reduced Fos expression following REMS-like state induced by pontine microinjections of a cholinergic agonist, carbachol in urethane-anesthetized rats. The percentage of Fos-positive TH cells was negatively correlated with the cumulative duration of REMS-like episodes induced during 140 min prior to brain harvesting in the A7 and rostral A5 groups bilaterally (p<0.01 for both), and in SubC neurons on the side opposite to carbachol injection (p<0.05). Dorsal medullary A2/C2 neurons did not exhibit such correlation, but their Fos expression (and that in A7, rostral A5 and SubC neurons) was positively correlated with the duration of the interval between the last REMSlike episode and the time of sacrifice (p<0.05). In contrast, neither of these correlations was significant for A1/C1 or caudal A5 neurons. These findings suggest that, similar to the prototypic LC neurons, neurons of the A7, rostral A5 and A2/C2 groups have reduced or abolished activity during REMS, whereas A1/C1 and caudal A5 neurons do not have this feature. The reduced during REMS activity in A2/C2, A5 and A7 neurons, and the associated decrements in norepinephrine release, may cause state-dependent modulation of transmission in brain somato-and viscerosensory, somatomotor, and cardiorespiratory pathways.Keywords autonomic regulation; brainstem; locus coeruleus; motor control; norepinephrine *Corresponding author: Irma Rukhadze, Ph.D., Department of Animal Biology 209E/VET, School of Veterinary Medicine, University of Pennsylvania, 3800 Spruce Street, Philadelphia, PA 19104-6046, USA, Tel. +215-898-6489, Fax. +215-573-5186 E-mail: rukhadze@vet.upenn.edu (I. Rukhadze). Suggested Neuroscience Section Editor (Systems Neuroscience): Dr. Miles Herkenham, NIMH, Section on Functional Neuroanatomy, Bldg. 36, Rm. 2D15, 36, Convent Dr., MSC 4070, Bethesda, MD 20892-4070, USA.Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. NIH Public Ac...

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Section: Temporal Distribution and Cumulative Duration Of Rems-like Ementioning

confidence: 82%

Section: Temporal Distribution and Cumulative Duration Of Rems-like Ementioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats

et al. 2008

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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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Optogenetic Probing of Hypocretins’ Regulation of Wakefulness

Adamantidis

Lecea²

2011

Narcolepsy

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Disinhibition of perifornical hypothalamic neurones activates noradrenergic neurones and blocks pontine carbachol‐induced REM sleep‐like episodes in rats

Cited by 31 publications

References 59 publications

Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats

Fos expression in pontomedullary catecholaminergic cells following rapid eye movement sleep-like episodes elicited by pontine carbachol in urethane-anesthetized rats

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

Optogenetic Probing of Hypocretins’ Regulation of Wakefulness

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