scholarly journals Optical imaging of the ventral medullary surface across sleep-wake states

1999 ◽  
Vol 277 (4) ◽  
pp. R1239-R1245 ◽  
Author(s):  
C. A. Richard ◽  
D. M. Rector ◽  
R. K. Harper ◽  
R. M. Harper

We hypothesized that spontaneous activity declines over widespread areas of the cat ventral medullary surface (VMS) during rapid eye movement (REM) sleep. We assessed neural and hemodynamic activity, measured as changes in reflected 660- and 560-nm wavelength light, from the VMS during sleep and waking states in five adult, unrestrained cats and in two control cats. Relative to quiet sleep, overall activity declined, and variability, assessed by standard deviation, increased by 25% during REM sleep. Variability in activity during waking also increased by 45% over quiet sleep, but mean activity was unchanged. REM sleep onset was preceded by a reduction in the hemodynamic signal from 5 to 60 s before neural activity decline. The activity decline during REM sleep, previously noted in the goat rostral VMS, extends to intermediate VMS areas of the cat and differs from most neural sites, such as the cortex, hippocampus, and thalamus, which increase activity during REM sleep. The activity decline during REM sleep has the potential to modify VMS responsiveness to baroreceptor and chemoreceptor challenges during the REM state.

2000 ◽  
Vol 278 (4) ◽  
pp. R1090-R1098 ◽  
Author(s):  
D. M. Rector ◽  
C. A. Richard ◽  
R. J. Staba ◽  
R. M. Harper

Ventral medullary surface (VMS) activity declines during rapid eye movement (REM) sleep, suggesting a potential for reduced VMS responsiveness to blood pressure challenges during that state. We measured VMS neural activity, assessed as changes in reflected 660-nm wavelength light, during pressor and depressor challenges within sleep/waking states in five adult, unrestrained, unanesthetized cats and in two control cats. Phenylephrine elevated blood pressure and elicited an initial VMS activity decline and a subsequent rise in VMS activity in all states, although the initial decline during quiet sleep occurred only in rostral placements. Phasic REM periods elicited a momentary recovery from the evoked activity rise, and arousals diminished the overall elevation in activity. A sodium nitroprusside depressor challenge increased VMS activity more in REM sleep than in quiet sleep, with the increase being even less in waking. Enhanced responses to depressor challenges during REM sleep suggest a loss of dampening of evoked activity during that state; state-related differential baroreflex sensitivity may result from sleep-waking changes in VMS responses to blood pressure challenges.


1991 ◽  
Vol 260 (4) ◽  
pp. H1283-H1289 ◽  
Author(s):  
R. S. Horne ◽  
N. D. De Preu ◽  
P. J. Berger ◽  
A. M. Walker

Newborn lambs were subjected to hypertensive stimuli of 1-min duration to examine features of hypertension-induced arousal from sleep. Reflex mechanisms involved were studied by performing the same tests after sinoaortic denervation (SAD). In intact lambs, hypertension increased the probability of arousal from both quiet sleep (QS) and rapid-eye-movement (REM) sleep. Hypertension resulted in arousal in 51% (QS) and 50% (REM) of tests. Arousal time was significantly longer in REM (29.3 +/- 0.9 s, mean +/- SE) than in QS (22.6 +/- 0.6 s, P less than 0.01). Arterial oxygen saturation (So2) and partial pressure of oxygen (Po2) measured at the point of arousal, or after 60 s if arousal failed to occur, were unchanged from control values. After SAD hypertension did not increase the probability of arousal. Arousals significantly decreased (P less than 0.001) to 31% (QS) and 10% (REM). These findings indicate that acute hypertension, mediated via arterial baroreceptors, is a potent stimulus for arousal. In intact lambs, the arousal probability increased and arousal time decreased with increasing stimulus strength (1-30 mmHg), but the arousal time difference between QS and REM remained constant. Consideration of these findings in terms of a simple baroreflex threshold model suggests that the slower response in REM sleep is explained by slower neural processes after the achievement of a critical arousal input rather than by a higher threshold for baroreceptor input in this state.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A476-A476
Author(s):  
J L Sanchez ◽  
S Saeed ◽  
H Battistini

Abstract Introduction Agrypnia Excitata (AE) is a syndrome characterized by loss of sleep with permanent motor and autonomic hyper activation. This case describes this peculiar syndrome in a patient with paraneoplastic autoimmune encephalitis. Report of Case DG is a 35 yr old male with a history of anti-Ma2 limbic encephalitis secondary to cystic teratoma of the left testis diagnosed 6 months prior to presenting in Sleep Clinic. His parents described significant sleep disturbances including short sleep and wake periods throughout the day and night with no apparent pattern, acting out dreams, motor activity during sleep including pulling at his clothes or using his hands to manipulate invisible objects. Additionally they described low-grade fevers, and severe hyperphagia. Polysomnogram showed absence of slow-wave sleep and what appeared to be an admixture of stage 1 non-rapid eye movement (NREM) with rapid-eye movement (REM) sleep. Multiple sleep-latency testing (MSLT) demonstrated a mean sleep latency of 5.2 minutes and four sleep-onset REM periods (SOREMPs). Magnetic resonance imaging of the brain revealed persistent inflammation of the mesial temporal lobes and hippocampal region. Cerebral spinal fluid testing showed persistent anti-Ma2 antibodies. Based on this clinical presentation we made a diagnosis of Agrypnia Excitata. Conclusion Agrypnia Excitata is a syndrome characterized by loss of the normal sleep-wake rhythm. Sleep consists of the disappearance of spindle-delta activities, and persistent stage 1 NREM sleep mixed with recurrent episodes of REM sleep. The second hallmark of AE is persistent motor and autonomic hyperactivity observed during wake and sleep. AE has been described in three distinct clinical syndromes: Morvan Syndrome (autoimmune encephalitis), Fatal Familial Insomnia, and Delirium tremens. The pathogenesis of AE consists of intra-limbic disconnection releasing the hypothalamus and brainstem reticular formation from cortico-limbic inhibitory control. In autoimmune encephalitis, antibodies that act on voltage-gated potassium channels within the limbic system have been implicated in the pathophysiology.


2013 ◽  
Vol 36 (6) ◽  
pp. 610-611 ◽  
Author(s):  
Sen Cheng ◽  
Markus Werning

AbstractWe propose that rapid eye movement (REM) and slow-wave sleep contribute differently to the formation of episodic memories. REM sleep is important for building up invariant object representations that eventually recur to gamma-band oscillations in the neocortex. In contrast, slow-wave sleep is more directly involved in the consolidation of episodic memories through replay of sequential neural activity in hippocampal place cells.


2008 ◽  
Vol 295 (6) ◽  
pp. R2041-R2049 ◽  
Author(s):  
Joshi John ◽  
Lalini Ramanathan ◽  
Jerome M. Siegel

The histamine-containing posterior hypothalamic region (PH-TMN) plays a key role in sleep-wake regulation. We investigated rapid changes in glutamate release in the PH-TMN across the sleep-wake cycle with a glutamate biosensor that allows the measurement of glutamate levels at 1- to 4-s resolution. In the PH-TMN, glutamate levels increased in active waking (AW) and rapid eye movement (REM) sleep compared with quiet waking and nonrapid eye movement (NREM) sleep. There was a rapid (0.6 ± 1.8 s) and progressive increase in glutamate levels at REM sleep onset. A reduction in glutamate levels consistently preceded the offset of REM sleep by 8 ± 3 s. Short-duration sleep deprivation resulted in a progressive increase in glutamate levels in the PH-TMN, perifornical-lateral hypothalamus (PF-LH), and cortex. We found that in the PF-LH, glutamate levels took a longer time to return to basal values compared with the time it took for glutamate levels to increase to peak values during AW onset. This is in contrast to other regions we studied in which the return to baseline values after AW was quicker than their rise with waking onset. In summary, we demonstrated an increase in glutamate levels in the PH-TMN with REM/AW onset and a drop in glutamate levels before the offset of REM. High temporal resolution measurement of glutamate levels reveals dynamic changes in release linked to the initiation and termination of REM sleep.


2020 ◽  
Author(s):  
Carlos Blanco-Centurion ◽  
SiWei Luo ◽  
Aurelio Vidal-Ortiz ◽  
Priyattam J. Shiromani

AbstractSleep and wake are opposing behavioral states controlled by the activity of specific neurons. The neurons responsible for sleep/wake control have not been fully identifed due to the lack of in-vivo high throughput technology. We use the deep-brain calcium (Ca2+) imaging method to identify activity of hypothalamic neurons expressing the vesicular GABA transporter (vGAT), a marker of GABAergic neurons. vGAT-cre mice (n=5) were microinjected with rAAV-FLEX-GCaMP6M into the lateral hypothalamus and 21d later the Ca2+ influx in vGAT neurons (n=372) was recorded in freely-behaving mice during waking (W), NREM and REM sleep. Post-mortem analysis revealed the lens tip located in the zona incerta/lateral hypothalamus (ZI-LH) and the change in fluorescence of neurons in the field of view was as follows: 54.9% of the vGAT neurons had peak fluorescence during REM sleep (REM-max), 17.2% were NREM-max, 22.8% were wake-max while 5.1% were both wake+REM max. Thus, three quarters of the recorded vGAT neurons in the ZI-LH were most active during sleep. In the NREM-max group Ca2+ fluorescence anticipated the initiation of NREM sleep onset and remained high throughout sleep (NREM and REM sleep). In the REM-max neurons Ca2+fluorescence increased before the onset of REM sleep and stayed elevated during the episode. Activation of the vGAT NREM-max neurons in the zona incerta and dorsal lateral hypothalamus would inhibit the arousal neurons to initiate and maintain sleep.


1979 ◽  
Vol 47 (2) ◽  
pp. 279-284 ◽  
Author(s):  
N. Muller ◽  
G. Volgyesi ◽  
L. Becker ◽  
M. H. Bryan ◽  
A. C. Bryan

It is generally believed that there is a scarcity of muscle spindles in the diaphragm and that there is no tonic activity at end expiration. This conclusion is based mainly on animal studies and the difficulty in differentiating tonic electromyogram activity from noise. We have, however, found a number of muscle spindles in the newborn human diagphragm, concentrated in the region of the central tendon. We also tried to detect tonic activity by decreasing it (by rapid-eye movement (REM) sleep or anesthesia) or increasing it (with abdominal loading). During REM sleep in five infants and five adults, using subcostal electrodes were observed a marked fall in tonic activity (P less than 0.001) compared to non-REM or quiet sleep. We also observed a reduction in diaphragmatic tonic activity with halothane anesthesia (P less than 0.001). With esophageal electrodes in adult subjects, there was a rise in tonic diaphragmatic activity proportional to the amount of abdomina load (P less than 0.001). We conclude that there are muscle spindles in the human diaphragm and that there is tonic activity at end expiration.


PEDIATRICS ◽  
1976 ◽  
Vol 57 (1) ◽  
pp. 142-147
Author(s):  
M. Gabriel ◽  
M. Albani ◽  
F. J. Schulte

The incidence of apneic spells during different sleep states, active sleep, quiet sleep, and undifferentiated sleep was determined in eight preterm infants of 30 to 35 weeks' conceptional age, by means of a polygraphic recording technique. They were free of perinatal and postnatal complications other than apnea. During their active or rapid eye movement (REM) sleep they showed significantly more apneic episodes which were also longer lasting and they were accompanied by bradycardia of a greater severity. The organization of the immature nervous system with a preponderance of inhibitory synaptic connections and the additional inhibition of spinal motoneurons during REM sleep are likely to be the cause of apneic spells in otherwise "normal" preterm infants.


1992 ◽  
Vol 1 (4) ◽  
pp. 245-250 ◽  
Author(s):  
MEHDI TAFTI ◽  
ERIC VILLEMIN ◽  
BERTRAND CARLANDER ◽  
ALAIN BESSET ◽  
MICHEL BILLIARD

2020 ◽  
Author(s):  
Benjamin Stucky ◽  
Ian Clark ◽  
Yasmine Azza ◽  
Walter Karlen ◽  
Peter Achermann ◽  
...  

BACKGROUND Multisensor fitness trackers offer the ability to longitudinally estimate sleep quality in a home environment with the potential to outperform traditional actigraphy. To benefit from these new tools for objectively assessing sleep for clinical and research purposes, multisensor wearable devices require careful validation against the gold standard of sleep polysomnography (PSG). Naturalistic studies favor validation. OBJECTIVE This study aims to validate the Fitbit Charge 2 against portable home PSG in a shift-work population composed of 59 first responder police officers and paramedics undergoing shift work. METHODS A reliable comparison between the two measurements was ensured through the data-driven alignment of a PSG and Fitbit time series that was recorded at night. Epoch-by-epoch analyses and Bland-Altman plots were used to assess sensitivity, specificity, accuracy, the Matthews correlation coefficient, bias, and limits of agreement. RESULTS Sleep onset and offset, total sleep time, and the durations of rapid eye movement (REM) sleep and non–rapid-eye movement sleep stages N1+N2 and N3 displayed unbiased estimates with nonnegligible limits of agreement. In contrast, the proprietary Fitbit algorithm overestimated REM sleep latency by 29.4 minutes and wakefulness after sleep onset (WASO) by 37.1 minutes. Epoch-by-epoch analyses indicated better specificity than sensitivity, with higher accuracies for WASO (0.82) and REM sleep (0.86) than those for N1+N2 (0.55) and N3 (0.78) sleep. Fitbit heart rate (HR) displayed a small underestimation of 0.9 beats per minute (bpm) and a limited capability to capture sudden HR changes because of the lower time resolution compared to that of PSG. The underestimation was smaller in N2, N3, and REM sleep (0.6-0.7 bpm) than in N1 sleep (1.2 bpm) and wakefulness (1.9 bpm), indicating a state-specific bias. Finally, Fitbit suggested a distribution of all sleep episode durations that was different from that derived from PSG and showed nonbiological discontinuities, indicating the potential limitations of the staging algorithm. CONCLUSIONS We conclude that by following careful data processing processes, the Fitbit Charge 2 can provide reasonably accurate mean values of sleep and HR estimates in shift workers under naturalistic conditions. Nevertheless, the generally wide limits of agreement hamper the precision of quantifying individual sleep episodes. The value of this consumer-grade multisensor wearable in terms of tackling clinical and research questions could be enhanced with open-source algorithms, raw data access, and the ability to blind participants to their own sleep data.


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