scholarly journals Sleep spindles are resilient to extensive white matter deterioration

2020 ◽  
Vol 2 (2) ◽  
Author(s):  
Erlan Sanchez ◽  
Caroline Arbour ◽  
Héjar El-Khatib ◽  
Karine Marcotte ◽  
Hélène Blais ◽  
...  
Keyword(s):  
White Matter ◽  
Eye Movement ◽  
Control Group ◽  
Sleep Spindles ◽  
Rapid Eye Movement ◽  
Sleep Spindle ◽  
Rapid Eye Movement Sleep ◽  
Brain Injured ◽  
Healthy Control ◽  
The Brain

Abstract Sleep spindles are an essential part of non-rapid eye movement sleep, notably involved in sleep consolidation, cognition, learning and memory. These oscillatory waves depend on an interaction loop between the thalamus and the cortex, which relies on a structural backbone of thalamo-cortical white matter tracts. It is still largely unknown if the brain can properly produce sleep spindles when it underwent extensive white matter deterioration in these tracts, and we hypothesized that it would affect sleep spindle generation and morphology. We tested this hypothesis with chronic moderate to severe traumatic brain injury (n = 23; 30.5 ± 11.1 years old; 17 m/6f), a unique human model of extensive white matter deterioration, and a healthy control group (n = 27; 30.3 ± 13.4 years old; 21m/6f). Sleep spindles were analysed on a full night of polysomnography over the frontal, central and parietal brain regions, and we measured their density, morphology and sigma-band power. White matter deterioration was quantified using diffusion-weighted MRI, with which we performed both whole-brain voxel-wise analysis (Tract-Based Spatial Statistics) and probabilistic tractography (with High Angular Resolution Diffusion Imaging) to target the thalamo-cortical tracts. Group differences were assessed for all variables and correlations were performed separately in each group, corrected for age and multiple comparisons. Surprisingly, although extensive white matter damage across the brain including all thalamo-cortical tracts was evident in the brain-injured group, sleep spindles remained completely undisrupted when compared to a healthy control group. In addition, almost all sleep spindle characteristics were not associated with the degree of white matter deterioration in the brain-injured group, except that more white matter deterioration correlated with lower spindle frequency over the frontal regions. This study highlights the resilience of sleep spindles to the deterioration of all white matter tracts critical to their existence, as they conserve normal density during non-rapid eye movement sleep with mostly unaltered morphology. We show that even with such a severe traumatic event, the brain has the ability to adapt or to withstand alterations in order to conserve normal sleep spindles.

Influenza virus-induced sleep responses in mice with targeted disruptions in neuronal or inducible nitric oxide synthases

2004 ◽  
Vol 97 (1) ◽  
pp. 17-28 ◽  
Author(s):  
Lichao Chen ◽  
Deborah Duricka ◽  
Scott Nelson ◽  
Sanjib Mukherjee ◽  
Stewart G. Bohnet ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Eye Movement ◽  
Expression Profiles ◽  
Gene Expression Profiles ◽  
No Synthase ◽  
Cytokine Gene Expression ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
The Brain

Influenza viral infection induces increases in non-rapid eye movement sleep and decreases in rapid eye movement sleep in normal mice. An array of cytokines is produced during the infection, and some of them, such as IL-1β and TNF-α, are well-defined somnogenic substances. It is suggested that nitric oxide (NO) may mediate the sleep-promoting effects of these cytokines. In this study, we use mice with targeted disruptions of either the neuronal NO synthase (nNOS) or the inducible NO synthase (iNOS) gene, commonly referred to as nNOS or iNOS knockouts (KOs), to investigate sleep changes after influenza viral challenge. We report that the magnitude of viral-induced non-rapid eye movement sleep responses in both nNOS KOs and iNOS KOs was less than that of their respective controls. In addition, the duration of rapid eye movement sleep in nNOS KO mice did not decrease compared with baseline values. All strains of mice had similar viral titers and cytokine gene expression profiles in the lungs. Virus was not isolated from the brains of any strain. However, gene expression in the brain stem differed between nNOS KOs and their controls: mRNA for the interferon-induced gene 2′,5′-oligoadenylate synthase 1a was elevated in nNOS KOs relative to their controls at 15 h, and IL-1β mRNA was elevated in nNOS KOs relative to their controls at 48 h. Our results suggest that NO synthesized by both nNOS and iNOS plays a role in virus-induced sleep changes and that nNOS may modulate cytokine expression in the brain.

A cyclooxygenase-2 inhibitor attenuates spontaneous and TNF-α-induced non-rapid eye movement sleep in rabbits

2003 ◽  
Vol 285 (1) ◽  
pp. R99-R109 ◽  
Author(s):  
Hitoshi Yoshida ◽  
Takeshi Kubota ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Tnf Α ◽  
Cox 2 ◽  
The Brain

Sleep is regulated in part by the brain cytokine network, including tumor necrosis factor-α (TNF-α). TNF-α activates the transcription factor nuclear factor-κB, which in turn promotes transcription of many genes, including cyclooxygenase-2 (COX-2). COX-2 is in the brain and is an enzyme responsible for production of prostaglandin D2. The hypothesis that central COX-2 plays a role in the regulation of spontaneous and TNF-α-induced sleep was investigated. Three doses (0.5, 5, and 50 μg) of NS-398, a highly selective COX-2 inhibitor, were injected intracerebroventricularly. The highest dose decreased non-rapid eye movement sleep. The intermediate and highest doses decreased electroencephalographic slow-wave activity; the greatest reduction occurred after 50 μg of NS-398 during the first 3-h postinjection period. Rapid eye movement sleep and brain temperature were not altered by any dose of NS-398. Pretreatment of rabbits with 5 or 50 μg of NS-398 blocked the TNF-α-induced increases in non-rapid eye movement sleep, electroencephalographic slow-wave activity, and brain temperature. These data suggest that COX-2 is involved in the regulation of spontaneous and TNF-α-induced sleep.

scholarly journals Effects of oral temazepam on sleep spindles during non-rapid eye movement sleep: A high-density EEG investigation

2015 ◽  
Vol 25 (10) ◽  
pp. 1600-1610 ◽  
Author(s):  
D.T. Plante ◽  
M.R. Goldstein ◽  
J.D. Cook ◽  
R. Smith ◽  
B.A. Riedner ◽  
...  
Keyword(s):  
Eye Movement ◽  
High Density ◽  
Sleep Spindles ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

scholarly journals Alterations in sleep, sleep spindle, and EEG power in mGluR5 knockout mice

2020 ◽  
Vol 123 (1) ◽  
pp. 22-33 ◽  
Author(s):  
David D. Aguilar ◽  
Robert E. Strecker ◽  
Radhika Basheer ◽  
James M. McNally
Keyword(s):  
Eye Movement ◽  
Metabotropic Glutamate Receptor ◽  
Neural Oscillations ◽  
Alpha Power ◽  
Rapid Eye Movement ◽  
Sleep Spindle ◽  
Rapid Eye Movement Sleep ◽  
Metabotropic Glutamate ◽  
Gamma Power ◽  
Abnormal Sleep

The type 5 metabotropic glutamate receptor (mGluR5) represents a novel therapeutic target for schizophrenia and other disorders. Schizophrenia is associated with progressive abnormalities in cortical oscillatory processes including reduced spindles (8–15 Hz) during sleep and increased delta (0.5–4 Hz)- and gamma-band activity (30–80 Hz) during wakefulness. mGluR5 knockout (KO) mice demonstrate many schizophrenia-like behaviors, including abnormal sleep. To examine the effects of mGluR5 on the maintenance of the neocortical circuitry responsible for such neural oscillations, we analyzed sleep/wake electroencephalographic (EEG) activity of mGluR5 KO mice at baseline, after 6 h of sleep deprivation, and during a visual method of cortical entrainment (visual steady state response). We hypothesized mGluR5-KO mice would exhibit translationally relevant abnormalities in sleep and neural oscillations that mimic schizophrenia. Power spectral and spindle density analyses were performed across 24-h EEG recordings in mGluR5-KO mice and wild-type (WT) controls. Novel findings in mGluR5 KO mice include deficits in sleep spindle density, wake alpha power, and 40-Hz visual task-evoked gamma power and phase locking. Sigma power (10–15 Hz), an approximation of spindle activity, was also reduced during non-rapid eye movement sleep transitions. Our observations on abnormal sleep/wake are generally in agreement with previous reports, although we did not replicate changes in rapid eye movement sleep. The timing of these phenotypes may suggest an impaired circadian process in mGluR5 KO mice. In conclusion, EEG phenotypes in mGluR5 KO mice resemble deficits observed in patients with schizophrenia. These findings implicate mGluR5-mediated pathways in several translationally relevant phenotypes associated with schizophrenia, and suggest that agents targeting this receptor may have harmful consequences on sleep health and daily patterns of EEG power. NEW & NOTEWORTHY Metabotropic glutamate receptor type 5 (mGluR5) knockout (KO) mice show several translationally relevant abnormalities in neural oscillatory activity associated with schizophrenia. These include deficits in sleep spindle density, sigma and alpha power, and 40-Hz task-evoked gamma power. The timing of these phenotypes suggests an impaired circadian process in these mice. Previously reported rapid eye movement sleep deficits in this model were not observed. These findings suggest mGluR5-enhancing drugs may improve sleep stability and sleep spindle density, which could impact memory and cognition.

Startle-evoked changes in diaphragmatic activity during wakefulness and sleep

1990 ◽  
Vol 68 (1) ◽  
pp. 166-173 ◽  
Author(s):  
L. R. Kline ◽  
J. C. Hendricks ◽  
D. A. Silage ◽  
A. R. Morrison ◽  
R. O. Davies ◽  
...  
Keyword(s):  
Eye Movement ◽  
Startle Response ◽  
Moving Average ◽  
Respiratory Muscles ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Neural Basis ◽  
Excitatory Response ◽  
Muscle Atonia ◽  
The Brain

Tonic inhibition of some respiratory muscles occurs as part of the generalized muscle atonia of rapid-eye-movement sleep (REMS). A second type of inhibition of the diaphragm during REMS, fractionations, consists of brief pauses in the diaphragmatic electromyogram (DIA EMG) in association with phasic events. Because motor inhibition can occur as part of the startle response, and the brain is highly activated during REMS, we hypothesized that the neural basis of the fractionations might be activation of a startle network. To test this hypothesis, tone bursts (100 dB, 20-ms duration at 15-s intervals) were applied to cats at a fixed inspiratory level in the DIA moving average during REMS, non-rapid-eye-movement sleep (NREMS), and wakefulness. Parallel sham studies (no tone applied) were obtained for each state. The response of the DIA EMG was averaged over 100 ms by using the tone pulse as a trigger, and the following parameters of the DIA EMG were measured: latency to peak and/or nadir, increment or decrement in activity, and duration of peak and/or nadir. After a tone, all five animals studied displayed a profound suppression of DIA activity during REMS (latency to nadir 42.4 +/- 10.0 ms, duration of suppression 35.9 +/- 17.6 ms). Similarly, DIA activity was suppressed in all cats during NREMS (latency to nadir 40.9 +/- 13.3 ms, duration 23.9 +/- 13.4 ms). An excitatory response was observed in only two cats during NREMS and wakefulness. The similarity of startle-induced DIA EMG pauses to spontaneous fractionations of DIA activity during REMS suggests that the latter result from activation of a central startle system.

Subdiaphragmatic vagotomy blocks the sleepand fever-promoting effects of interleukin-1β

1997 ◽  
Vol 273 (4) ◽  
pp. R1246-R1253 ◽  
Author(s):  
Michael K. Hansen ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Brain Temperature ◽  
Alternative Pathway ◽  
Intraperitoneal Administration ◽  
Vagal Afferents ◽  
Interleukin 1Β ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
The Central Nervous System ◽  
The Brain

The mechanism by which peripheral cytokines signal the central nervous system to elicit central manifestations of the acute phase response remains unknown. Recent evidence suggests that cytokines may signal the brain via the vagus nerve. To test this possibility, we examined sleep-wake activity and brain temperature (Tbr) after the intraperitoneal administration of saline or three doses (0.1, 0.5, and 2.5 μg/kg) of interleukin-1β (IL-1β) in subdiaphragmatically vagotomized (Vx) and sham-operated (Sham) rats. The lowest dose of IL-1β (0.1 μg/kg) increased non-rapid eye movement sleep (NREMS) and slightly elevated Tbr in Sham rats; both responses were blocked in Vx animals. The middle dose tested (0.5 μg/kg) increased NREMS and Tbr in Sham animals; however, in Vx rats, the increase in NREMS was attenuated and the increase in Tbr was blocked. The highest dose of IL-1β used (2.5 μg/kg) induced increases in NREMS, decreases in rapid eye movement sleep, and a hypothermic response followed by a biphasic fever; these responses were similar in both Sham and Vx rats. These data provide strong evidence that the subdiaphragmatic vagus plays an important role in communicating both sleep and fever signals to the brain. However, there is clearly an alternative pathway by which IL-1 can signal the brain; whether it occurs through activation of other vagal afferents or through direct or indirect actions on the brain remains unknown.

Case Report: Polysomnographic Effects of Thalamotomy for Torsion Dystonia

Neurosurgery ◽  
1984 ◽  
Vol 14 (4) ◽  
pp. 495-498 ◽  
Author(s):  
William R. Jankel ◽  
Ernst Niedermeyer ◽  
Martin Graf ◽  
Michael J. Kalsher
Keyword(s):  
Eye Movement ◽  
High Amplitude ◽  
Common Mechanism ◽  
Sleep Spindles ◽  
Poor Sleep ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Torsion Dystonia ◽  
Continuous Type ◽  
Sleep Parameters

Abstract We report a patient with torsion dystonia whose polysomnographic recordings revealed poor sleep and a pronounced and almost continuous type of spindle activity during non-rapid eye movement sleep. Rapid eye movement sleep was also reduced. These changes proved to be independent of medications. After a clinically successful unilateral thalamic operation, a normalization of sleep parameters and a reduction of the high amplitude sleep spindles was observed. implying that the regulation of sleep spindles and the advancement of dystonic symptoms are affected by a common mechanism.

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