scholarly journals Noradrenergic modulation of masseter muscle activity during natural rapid eye movement sleep requires glutamatergic signalling at the trigeminal motor nucleus

2014 ◽  
Vol 592 (16) ◽  
pp. 3597-3609 ◽  
Author(s):  
Peter B. Schwarz ◽  
Saba Mir ◽  
John H. Peever
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Masseter Muscle ◽  
Motor Nucleus ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Trigeminal Motor Nucleus ◽  
Noradrenergic Modulation

Respiratory motor activity: influence of neuromodulators and implications for sleep disordered breathingThis paper is one of a selection of papers published in this Special Issue, entitled Young Investigators' Forum.

2007 ◽  
Vol 85 (1) ◽  
pp. 155-165 ◽  
Author(s):  
Richard L. Horner
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Muscle Tone ◽  
Motor Nucleus ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Upper Airways ◽  
Pharyngeal Muscle ◽  
Pharyngeal Airway ◽  
Obstructive Sleep

Sleep, especially rapid-eye-movement sleep, causes fundamental modifications of respiratory muscle activity and control mechanisms, modifications that can predispose individuals to sleep-related breathing disorders. One of the most common of these disorders is obstructive sleep apnea (OSA) that affects approximately 4% of adults. OSA is caused by repeated episodes of pharyngeal airway obstruction that can occur hundreds of times per night, leading to recurrent asphyxia, arousals from sleep, daytime sleepiness, and adverse cardiovascular and cerebrovascular consequences. OSA is caused by the effects of sleep on pharyngeal muscle tone in individuals with already narrow upper airways. Moreover, since OSA occurs only in sleep, this disorder by definition is a state-dependent process ultimately caused by the influence of sleep neural mechanisms on the activity of pharyngeal motoneurons. This review synthesizes recent findings relating to control of pharyngeal muscle activity across sleep–wake states, with special emphasis on the influence of neuromodulators acting at the hypoglossal motor nucleus that inervates the genioglossus muscle of the tongue. The results of such basic physiological studies may be relevant to identifying and developing new pharmacological strategies to augment pharyngeal muscle activity in sleep, especially rapid-eye-movement sleep, as potential treatments for OSA.

scholarly journals Comparison of rhythmic masticatory muscle activity during non-rapid eye movement sleep in guinea pigs and humans

2017 ◽  
Vol 27 (4) ◽  
pp. e12608 ◽  
Author(s):  
Takafumi Kato ◽  
Risa Toyota ◽  
Shingo Haraki ◽  
Hiroyuki Yano ◽  
Makoto Higashiyama ◽  
...  
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Guinea Pigs ◽  
Masticatory Muscle ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Rhythmic Masticatory Muscle Activity ◽  
Masticatory Muscle Activity

Disturbance of phasic chin muscle activity during rapid-eye-movement sleep

2001 ◽  
Vol 23 ◽  
pp. S104-S107 ◽  
Author(s):  
Jun Kohyama ◽  
Junko Ohinata ◽  
Takeshi Hasegawa
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

Excitatory Effects of Hypocretin-1 (Orexin-A) in the Trigeminal Motor Nucleus Are Reversed by NMDA Antagonism

2003 ◽  
Vol 89 (5) ◽  
pp. 2591-2600 ◽  
Author(s):  
John H. Peever ◽  
Yuan-Yang Lai ◽  
Jerome M. Siegel
Keyword(s):  
Muscle Activity ◽  
Masseter Muscle ◽  
Muscle Tone ◽  
Glutamate Release ◽  
Nmda Antagonist ◽  
Motor Nucleus ◽  
Dependent Manner ◽  
Orexin A ◽  
Trigeminal Motor Nucleus ◽  
Hypocretin 1

Hypocretin-1 and -2 (Hcrt-1 and -2, also called orexin-A and -B) are newly identified neuropeptides synthesized by hypothalamic neurons. Defects in the Hcrt system underlie the sleep disorder narcolepsy, which is characterized by sleep fragmentation and the involuntary loss of muscle tone called cataplexy. Hcrt neurons project to multiple brain regions including cranial and spinal motor nuclei. In vitro studies suggest that Hcrt application can modulate presynaptic glutamate release. Together these observations suggest that Hcrt can affect motor output and that glutamatergic processes may be involved. We addressed these issues in decerebrate cats by applying Hcrt-1 and -2 into the trigeminal motor nucleus to determine whether these ligands alter masseter muscle activity and by pretreating the trigeminal motor nucleus with a N-methyl-d-aspartate (NMDA) antagonist to determine if glutamatergic pathways are involved in the transduction of the Hcrt signal. We found that Hcrt-1 and -2 microinjections into the trigeminal motor nucleus increased ipsilateral masseter muscle tone in a dose-dependent manner. We also found that Hcrt application into the hypoglossal motor nucleus increases genioglossus muscle activity. Pretreatment with a NMDA antagonist (d-(−)-2-amino-phosphonovaleric acid) abolished the excitatory response of the masseter muscle to Hcrt-1 application; however, pretreatment with methysergide, a serotonin antagonist had no effect. These studies are the first to demonstrate that Hcrt causes the excitation of motoneurons and that functional NMDA receptors are required for this response. We suggest that Hcrt regulates motor control processes and that this regulation is mediated by glutamate release in the trigeminal motor nucleus.

scholarly journals Pentobarbital Dose-dependently Increases Respiratory Genioglossus Muscle Activity while Impairing Diaphragmatic Function in Anesthetized Rats

2009 ◽  
Vol 110 (6) ◽  
pp. 1327-1334 ◽  
Author(s):  
Matthias Eikermann ◽  
Philipp Fassbender ◽  
Sebastian Zaremba ◽  
Amy S. Jordan ◽  
Carl Rosow ◽  
...  
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Natural Sleep ◽  
Pentobarbital Anesthesia ◽  
Diaphragmatic Function ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Background Anesthetics depress both ventilatory and upper airway dilator muscle activity and thus put the upper airway at risk for collapse. However, these effects are agent-dependent and may involve upper airway and diaphragm muscles to varying degrees. The authors assessed the effects of pentobarbital on upper airway dilator and respiratory pump muscle function in rats and compared these results with the effects of normal sleep. Methods Tracheostomized rats were given increasing doses of pentobarbital to produce deep sedation then light and deep anesthesia, and negative pressure airway stimuli were applied (n = 11). To compare the effects of pentobarbital with those of natural sleep, the authors chronically instrumented rats (n = 10) with genioglossus and neck electromyogram and electroencephalogram electrodes and compared genioglossus activity during wakefulness, sleep (rapid eye movement and non-rapid eye movement), and pentobarbital anesthesia. Results Pentobarbital caused a dose-dependent decrease in ventilation and in phasic diaphragmatic electromyogram by 11 +/- 0.1%, but it increased phasic genioglossus electromyogram by 23 +/- 0.2%. Natural non-rapid eye movement sleep and pentobarbital anesthesia (10 mg/kg intraperitoneally) decreased respiratory genioglossus electromyogram by 61 +/- 29% and 45 +/- 35%, respectively, and natural rapid eye movement sleep caused the greatest decrease in phasic genioglossus electromyogram (95 +/- 0.3%). Conclusions Pentobarbital in rats impairs respiratory genioglossus activity compared to the awake state, but the decrease is no greater than seen during natural sleep. During anesthesia, in the absence of pharyngeal airflow, phasic genioglossus activity is increased in a dose-dependent fashion.

Submentalis Rapid Eye Movement Sleep Muscle Activity: A Potential Biomarker for Synucleinopathy

2019 ◽  
Vol 86 (6) ◽  
pp. 969-974 ◽  
Author(s):  
Stuart J. McCarter ◽  
John C. Feemster ◽  
Grace M. Tabatabai ◽  
David J. Sandness ◽  
Paul C. Timm ◽  
...  
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Potential Biomarker
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