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 ◽  
...  
SLEEP ◽  
2019 ◽  
Vol 43 (1) ◽  
Author(s):  
Brook L W Sweeten ◽  
Amy M Sutton ◽  
Laurie L Wellman ◽  
Larry D Sanford

Abstract Study Objectives To examine the rapid eye movement sleep (REM) response to mild stress as a predictor of the REM response to intense stress and brain-derived neurotrophic factor (BDNF) as a potential biomarker of stress resilience and vulnerability. Methods Outbred Wistar rats were surgically implanted with electrodes for recording electroencephalography (EEG) and electromyogram (EMG) and intraperitoneal Data loggers to record body temperature. Blood was also obtained to measure circulating BDNF. After recovery, rats were exposed to mild stress (novel chamber, NC) and later intense stress (shock training, ST), followed by sleep recording. Subsequently, rats were separated into resilient (Res; n=27) or vulnerable (Vul; n = 15) based on whether or not there was a 50% or greater decrease in REM after ST compared to baseline. We then compared sleep, freezing, and the stress response (stress-induced hyperthermia, SIH) across groups to determine the effects of mild and intense stress to determine if BDNF was predictive of the REM response. Results REM totals in the first 4 hours of sleep after exposure to NC predicted REM responses following ST with resilient animals having higher REM and vulnerable animals having lower REM. Resilient rats had significantly higher baseline peripheral BDNF compared to vulnerable rats. Conclusions These results show that outbred rats display significant differences in post-stress sleep and peripheral BDNF identifying these factors as potential markers of resilience and vulnerability prior to traumatic stress.


2017 ◽  
Vol 27 (4) ◽  
pp. e12608 ◽  
Author(s):  
Takafumi Kato ◽  
Risa Toyota ◽  
Shingo Haraki ◽  
Hiroyuki Yano ◽  
Makoto Higashiyama ◽  
...  

2001 ◽  
Vol 23 ◽  
pp. S104-S107 ◽  
Author(s):  
Jun Kohyama ◽  
Junko Ohinata ◽  
Takeshi Hasegawa

2007 ◽  
Vol 85 (1) ◽  
pp. 155-165 ◽  
Author(s):  
Richard L. Horner

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.


2009 ◽  
Vol 110 (6) ◽  
pp. 1327-1334 ◽  
Author(s):  
Matthias Eikermann ◽  
Philipp Fassbender ◽  
Sebastian Zaremba ◽  
Amy S. Jordan ◽  
Carl Rosow ◽  
...  

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.


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