Role of corticotropin-releasing hormone in stressor-induced alterations of sleep in rat

2002 ◽  
Vol 283 (2) ◽  
pp. R400-R407 ◽  
Author(s):  
Fang-Chia Chang ◽  
Mark R. Opp
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Brain Temperature ◽  
Physical Restraint ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Central Administration ◽  
Corticotropin Releasing Hormone ◽  
Releasing Hormone ◽  
The Impact

Corticotropin-releasing hormone (CRH) mediates responses to a variety of stressors. We subjected rats to a 1-h period of an acute stressor, physical restraint, and determined the impact on subsequent sleep-wake behavior. Restraint at the beginning of the light period, but not the dark period, increased waking and reduced rapid eye movement sleep without dramatically altering slow-wave sleep (SWS). Electroencephalogram (EEG) slow-wave activity during SWS and brain temperature were increased by this manipulation. Central administration of the CRH receptor antagonist astressin blocked the increase in waking after physical restraint, but not during the period of restraint itself. Blockade of CRH receptors with astressin attenuated the restraint-induced elevation of brain temperature, but not the increase of EEG slow-wave activity during subsequent SWS. Although corticosterone increased after restraint in naive animals, it was not altered by this manipulation in rats well habituated to handling and injection procedures. These results suggest that under these conditions central CRH, but not the hypothalamic-pituitary-adrenal axis, is involved in the alterations in sleep-wake behavior and the modulation of brain temperature of rats exposed to physical restraint.

Growth hormone-releasing hormone antibodies suppress sleep and prevent enhancement of sleep after sleep deprivation

1992 ◽  
Vol 263 (5) ◽  
pp. R1078-R1085 ◽  
Author(s):  
F. Obal ◽  
L. Payne ◽  
M. Opp ◽  
P. Alfoldi ◽  
L. Kapas ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Slow Wave ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Base Line ◽  
Light Cycle ◽  
Growth Hormone Releasing Hormone ◽  
Releasing Hormone

Previous reports suggest that the hypothalamic growth hormone-releasing hormone (GHRH) promotes sleep, especially non-rapid-eye-movement sleep (NREMS). To evaluate the role of endogenous GHRH in sleep regulation, the effects of antibodies to rat GHRH (GHRH-ab) were studied on normal sleep, brain temperature (Tbr), and GH secretion in experiment I and on enhanced sleep after sleep deprivation in experiment II. In experiment I, affinity-purified GHRH-ab (50 and 200 micrograms) raised in goats and a control goat immunoglobulin G (IgG) preparation were injected intracerebroventricularly (icv) in rats 1 h before the onset of the light cycle, and sleep-wake activity and Tbr were recorded for the next 12 or 23 h. Both doses of GHRH-ab suppressed NREMS and REMS throughout the light cycle. Sleep durations at night were normal. Electroencephalographic (EEG) slow-wave activity, characterized by EEG slow-wave amplitudes, was reduced after GHRH-ab during both the light and the dark cycles. Plasma GH concentrations measured 6-12 h after injection of GHRH-ab (200 micrograms) were diminished. Both the control IgG and GHRH-ab elicited fever. In experiment II, the sleep-wake activity and Tbr of rats were recorded for 24 h in three experimental conditions: base-line with icv injection of IgG, 3-h sleep deprivation with icv IgG injection, and 3-h sleep deprivation with icv GHRH-ab (200 micrograms). After sleep deprivation (+IgG), a prompt increase in EEG slow-wave activity (power density analysis) and late increases in NREMS and REMS durations were found.(ABSTRACT TRUNCATED AT 250 WORDS)

EEG delta power and auditory arousal in rested and sleep-deprived rabbits

1997 ◽  
Vol 272 (2) ◽  
pp. R648-R655 ◽  
Author(s):  
M. R. Opp ◽  
L. A. Toth ◽  
E. A. Tolley
Keyword(s):  
Slow Wave ◽  
Slow Wave Sleep ◽  
Rabbit Model ◽  
Stimulus Presentation ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Auditory Stimuli ◽  
Delta Power ◽  
Postural Changes ◽  
Behavioral Responsiveness

Slow-wave activity in the electroencephalogram is thought to reflect the depth or intensity of sleep. This hypothesis is primarily derived from studies of rats or humans. However, some characteristics of sleep of rabbits differ from those of rats or humans. To determine whether slow-wave activity (power density in the delta frequency band of 0.5-5.0 Hz) correlates with arousability in rabbits, we presented auditory stimuli (72-90 dB) to control or sleep-deprived animals during slow-wave sleep. The resulting behavioral responses, defined by changes in eye state and body posture, and the latency to return to sleep were used as measures of arousability. Behavioral responsiveness to auditory stimuli increased with increasing stimulus intensity in both control and sleep-deprived animals. Overall, however, sleep-deprived animals exhibited fewer postural changes and eye openings than did control rabbits. Sleep-deprived rabbits also more rapidly returned to sleep after the stimulus presentation than did control animals. Latency to return to sleep was correlated with delta power before stimulus presentation, but behavioral responsiveness was not. These data suggest that, in this rabbit model, delta power may not be predictive of behavioral arousability but may reflect sleep propensity.

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 Scalp EEG interictal high frequency oscillations as an objective EEG biomarker of infantile spasms

2020 ◽  
Author(s):  
Hiroki Nariai ◽  
Shaun A. Hussain ◽  
Danilo Bernardo ◽  
Hirotaka Motoi ◽  
Masaki Sonoda ◽  
...  
Keyword(s):  
Slow Wave ◽  
High Frequency ◽  
Slow Wave Sleep ◽  
Wave Activity ◽  
Infantile Spasms ◽  
Slow Wave Activity ◽  
List Type ◽  
Normal Children ◽  
High Frequency Oscillations ◽  
Epileptic Spasms

ABSTRACTObjectiveTo investigate the diagnostic utility of high frequency oscillations (HFOs) via scalp electroencephalogram (EEG) in infantile spasms.MethodsWe retrospectively analyzed interictal slow-wave sleep EEGs sampled at 2,000 Hz recorded from 30 consecutive patients who were suspected of having infantile spasms. We measured the rate of HFOs (80-500 Hz) and the strength of the cross-frequency coupling between HFOs and slow-wave activity (SWA) at 3-4 Hz and 0.5-1 Hz as quantified with modulation indices (MIs).ResultsTwenty-three patients (77%) exhibited active spasms during the overnight EEG recording. Although the HFOs were detected in all children, increased HFO rate and MIs correlated with the presence of active spasms (p < 0.001 by HFO rate; p < 0.01 by MIs at 3-4 Hz; p = 0.02 by MIs at 0.5-1 Hz). The presence of active spasms was predicted by the logistic regression models incorporating HFO-related metrics (AUC: 0.80-0.98) better than that incorporating hypsarrhythmia (AUC: 0.61). The predictive performance of the best model remained favorable (87.5% accuracy) after a cross-validation procedure.ConclusionsIncreased rate of HFOs and coupling between HFOs and SWA are associated with active epileptic spasms.SignificanceScalp-recorded HFOs may serve as an objective EEG biomarker for active epileptic spasms.HighlightsObjective analyses of scalp high frequency oscillations and its coupling with slow-wave activity in infantile spasms were feasible.Increased rate of high frequency oscillations and its coupling with slow-wave activity correlated with active epileptic spasms.The scalp high frequency oscillations were also detected in neurologically normal children (although at the low rate).

Antagonism of corticotropin-releasing hormone alters serotonergic-induced changes in brain temperature, but not sleep, of rats

2005 ◽  
Vol 289 (4) ◽  
pp. R1116-R1123 ◽  
Author(s):  
Luca Imeri ◽  
Susanna Bianchi ◽  
Mark R. Opp
Keyword(s):  
Body Temperature ◽  
Time Course ◽  
Dark Period ◽  
Brain Temperature ◽  
Nrem Sleep ◽  
Corticotropin Releasing Hormone ◽  
Light Onset ◽  
Releasing Hormone ◽  
The Impact ◽  
Higher Doses

Serotonin is involved in many physiological processes, including the regulation of sleep and body temperature. Administration into rats of low doses (25, 50 mg/kg) of the 5-HT precursor l-5-hydroxytryptophan (5-HTP) at the beginning of the dark period of the 12:12-h light-dark cycle initially increases wakefulness. Higher doses (75, 100 mg/kg) increase nonrapid eye movement (NREM) sleep. The initial enhancement of wakefulness after low-dose 5-HTP administration may be a direct action of 5-HT in brain or due to 5-HT-induced activation of other arousal-promoting systems. One candidate arousal-promoting system is corticotropin-releasing hormone (CRH) and the hypothalamic-pituitary-adrenal axis. Serotonergic activation by 5-HTP at the beginning of the dark period also induces hypothermia. Because sleep and body temperature are influenced by circadian factors, one aim of this study was to determine responses to 5-HTP when administered at a different circadian time, the beginning of the light period. Results obtained show that all doses of 5-HTP (25–100 mg/kg) administered at light onset initially increase wakefulness; NREM sleep increases only after a long delay, during the subsequent dark period. Serotonergic activation by 5-HTP at light onset induces hypothermia, the time course of which is biphasic after higher doses (75, 100 mg/kg). Intracerebroventricular pretreatment with the CRH receptor antagonist α-helical CRH does not alter the impact of 5-HTP on sleep-wake behavior but potentiates the hypothermic response to 50 mg/kg 5-HTP. These data suggest that serotonergic activation by peripheral administration of 5-HTP may modulate sleep-wake behavior by mechanisms in addition to direct actions in brain and that circadian systems are important determinants of the impact of serotonergic activation on sleep and body temperature.

scholarly journals Vagotomy attenuates but does not prevent the somnogenic and febrile effects of lipopolysaccharide in rats

1998 ◽  
Vol 274 (2) ◽  
pp. R406-R411 ◽  
Author(s):  
Levente Kapás ◽  
Michael K. Hansen ◽  
Hee-Yoon Chang ◽  
James M. Krueger
Keyword(s):  
Vagus Nerve ◽  
Eye Movement ◽  
Slow Wave ◽  
Dark Period ◽  
Brain Temperature ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

The role of the vagus nerve in the somnogenic and pyrogenic effects of lipopolysaccharide (LPS) was studied in rats. Control rats ( n= 8) and rats subjected to bilateral subdiaphragmal vagotomy (VX; n = 9) were injected with 100 μg/kg ip LPS at the beginning of the dark period. Sleep and brain temperature (Tbr) were recorded for 23 h after the injections. LPS caused increases in non-rapid eye movement sleep (NREMS) for 12 h after the injection in control rats. Sleep intensity, as indicated by the slow-wave activity (SWA) of the electroencephalogram during NREMS, was suppressed. LPS elicited biphasic Tbr responses: an initial hypothermia was followed by increases in Tbr that lasted for ∼20 h. In vagotomized rats, the NREMS responses to LPS were blunted. The magnitude of the LPS-induced NREMS increases was about one-half of that seen in control rats, and these sleep responses lasted only for 6 h. LPS did not affect SWA in VX animals. VX completely abolished the hypothermic responses to LPS and shortened the duration of the hyperthermia. The results suggest that the subdiaphragmal vagi play an important, but not exclusive, role in the somnogenic and pyrogenic actions of intraperitoneally injected LPS.

scholarly journals The Impact of a 4-Hour Sleep Delay on Slow Wave Activity in Twins Discordant for Chronic Fatigue Syndrome

SLEEP ◽  
2007 ◽  
Vol 30 (5) ◽  
pp. 657-662 ◽  
Author(s):  
Roseanne Armitage ◽  
Carol Landis ◽  
Robert Hoffmann ◽  
Martha Lentz ◽  
Nathaniel F. Watson ◽  
...  
Keyword(s):  
Chronic Fatigue Syndrome ◽  
Slow Wave ◽  
Chronic Fatigue ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Fatigue Syndrome ◽  
The Impact

scholarly journals High-Resolution Spectral Sleep Analysis Reveals a Novel Association Between Slow Oscillations and Memory Retention in Elderly Adults

2021 ◽  
Vol 12 ◽  
Author(s):  
Makoto Kawai ◽  
Logan D. Schneider ◽  
Omer Linkovski ◽  
Josh T. Jordan ◽  
Rosy Karna ◽  
...  
Keyword(s):  
Older Adults ◽  
Slow Wave ◽  
Verbal Memory ◽  
Healthy Aging ◽  
Slow Wave Sleep ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Medium Effect ◽  
Memory Retention ◽  
Slow Oscillations

Objective: In recognition of the mixed associations between traditionally scored slow wave sleep and memory, we sought to explore the relationships between slow wave sleep, electroencephalographic (EEG) power spectra during sleep and overnight verbal memory retention in older adults.Design, Setting, Participants, and Measurements: Participants were 101 adults without dementia (52% female, mean age 70.3 years). Delayed verbal memory was first tested in the evening prior to overnight polysomnography (PSG). The following morning, subjects were asked to recall as many items as possible from the same List (overnight memory retention; OMR). Partial correlation analyses examined the associations of delayed verbal memory and OMR with slow wave sleep (SWS) and two physiologic EEG slow wave activity (SWA) power spectral bands (0.5–1 Hz slow oscillations vs. 1–4 Hz delta activity).Results: In subjects displaying SWS, SWS was associated with enhanced delayed verbal memory, but not with OMR. Interestingly, among participants that did not show SWS, OMR was significantly associated with a higher slow oscillation relative power, during NREM sleep in the first ultradian cycle, with medium effect size.Conclusions: These findings suggest a complex relationship between SWS and memory and illustrate that even in the absence of scorable SWS, older adults demonstrate substantial slow wave activity. Further, these slow oscillations (0.5–1 Hz), in the first ultradian cycle, are positively associated with OMR, but only in those without SWS. Our findings raise the possibility that precise features of slow wave activity play key roles in maintaining memory function in healthy aging. Further, our results underscore that conventional methods of sleep evaluation may not be sufficiently sensitive to detect associations between SWA and memory in older adults.

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