Evidence map›Paper›PMID 24746052›Full record

ArticleProgress in brain research2014

Sleep-wake control of the upper airway by noradrenergic neurons, with and without intermittent hypoxia.

Leszek Kubin

Abstract read
In one paragraph

Article in Progress in brain research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
5.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 21 citations in OpenAlex.

  1. Review
  2. Review
  3. Activity of pontine A7 noradrenergic neurons is suppressed during REM sleep.Journal of applied physiology (Bethesda, Md. : 1985) · 2022
    Article
  4. Article
  5. Article
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  7. Muscarinic Inhibition of Hypoglossal Motoneurons: Possible Implications for Upper Airway Muscle Hypotonia during REM Sleep.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  8. Article
  9. Review
  10. Article
  11. JCI insight · 2017
    Article
  12. Review
  13. Article
  14. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

1 author at 1 institution in 1 country.

Leszek KubinDepartment of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA. Electronic address: lkubin@vet.upenn.edu.
University of Pennsylvania · US

Funding

SCOR IN NEUROBIOLOGY SLEEP AND SLEEP APNEAP50HL060287 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI DAVIES, RICHARD O · 1998 to 2007
$17.2M
PREMOTOR CONTROL OF UPPER AIRWAY AND REM SLEEP ATONIAR01HL047600 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KUBIN, LESZEK K · 1992 to 2018
$5.6M
EPISODIC HYPOXIA, HYPOTHALAMUS AND INSULIN RESISTANCER01HL074385 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI KUBIN, LESZEK K · 2003 to 2007
$1.9M
NHLBI NIH HHS HL-47600NHLBI NIH HHS HL-60287NHLBI NIH HHS HL-74385NHLBI NIH HHS P50 HL060287NHLBI NIH HHS R01 HL047600NHLBI NIH HHS R01 HL074385
6 · The paper itself

Abstract

Hypoglossal (XII) motoneurons innervate muscles of the tongue whose tonic and inspiratory modulated activity protects the upper airway from collapse in patients affected by the obstructive sleep apnea (OSA) syndrome. Both norepinephrine and serotonin provide wakefulness-related excitatory drives that maintain activity in XII motoneurons, with the noradrenergic system playing a particularly prominent role in rats. When noradrenergic and serotonergic drives are antagonized, no further decline of XII nerve activity occurs during pharmacologically induced rapid eye movement (REM) sleep-like state. This is the best evidence to date that, at least in this model, the entire REM sleep-related decline of upper airway muscle tone results from withdrawal of these two excitatory inputs. A major component of noradrenergic input to XII motoneurons originates from pontine noradrenergic neurons that have state-dependent patterns of activity, maximal during wakefulness, and minimal, or absent during REM sleep. Our data suggest that not all ventrolateral medullary catecholaminergic neurons follow this pattern, with adrenergic C1 neurons probably increasing their activity during REM sleep. When rats are subjected to chronic-intermittent hypoxia, noradrenergic drive to XII motoneurons is increased by mechanisms that include sprouting of noradrenergic terminals in the XII nucleus, and increased expression of α1-adrenoceptors; an outcome that may underlie the elevated baseline activity of upper airway muscles during wakefulness in OSA patients.

Indexed as

Adrenergic NeuronsAnimalsHumansHypoglossal NerveHypoxiaMotor NeuronsRatsRespiratory SystemSleepSleep Apnea, ObstructiveWakefulnessadrenergic receptorsatoniagenioglossusnorepinephrineobstructive sleep apneaREM sleep

Identifiers

PMID24746052
PMCPMC4498577
OpenAlexW107323758

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.