Pregnancy-associated sleep changes in the rat

1996 ◽  
Vol 271 (4) ◽  
pp. R1063-R1069 ◽  
Author(s):  
M. Kimura ◽  
S. Q. Zhang ◽  
S. Inoue
Keyword(s):  
Sleep Disorder ◽  
Eye Movement ◽  
Brain Temperature ◽  
Early Period ◽  
Underlying Mechanism ◽  
Normal Pregnancy ◽  
Female Rats ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Before And After

Sleep disorder during the course of pregnancy has been recently recognized in humans. However, the underlying mechanism of pregnancy-associated sleep disorder remains undetermined, and sleep changes even during normal pregnancy have not been fully understood. To describe the effects of pregnancy on sleep, sleep-wake patterns before and after fertile mating were compared in an animal model. Baseline recordings of sleep and brain temperature were made throughout a normal 4-day estrous cycle in female rats. After the rats became pregnant, the recordings continued across the entire pregnant period. Compared with baseline sleep before mating, both non-rapid eye movement sleep and rapid eye movement sleep increased significantly from the first night of pregnancy. Although rapid eye movement sleep returned to the baseline level from midpregnancy, nocturnal non-rapid eye movement sleep stayed enhanced during the entire pregnant period. Daytime sleep fluctuated toward the end of pregnancy. Brain temperature was elevated during the early period of pregnancy but did not correlate with enhanced sleep. The results suggest that physiological changes in different stages of pregnancy may contribute to the regulation of maternal sleep and temperature.

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.

Inhibition of nitric oxide synthesis suppresses sleep in rabbits

1994 ◽  
Vol 266 (1) ◽  
pp. R151-R157 ◽  
Author(s):  
L. Kapas ◽  
M. Shibata ◽  
M. Kimura ◽  
J. M. Krueger
Keyword(s):  
Nitric Oxide ◽  
Eye Movement ◽  
Brain Temperature ◽  
Interleukin 1 ◽  
Systemic Blood Pressure ◽  
Common Mechanism ◽  
Rapid Eye Movement ◽  
Nitric Oxide Synthesis ◽  
Rapid Eye Movement Sleep ◽  
Intracerebroventricular Injections

The effects of N omega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthesis, on spontaneous and interleukin-1 (IL-1)-induced sleep were examined in rabbits. Animals were injected intracerebroventricularly or intravenously during the light phase with vehicle, L-NAME, IL-1, or the combination of L-NAME and IL-1. Injection of L-NAME (5 mg icv and 100 mg/kg iv) suppressed both non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS) for 4-6 h. The sleep-suppressive effects are unlikely due to pressor responses to L-NAME because administration of L-NAME (5 mg icv) produced only a transient (3-4 min) slight increase in systemic blood pressure. Injection of IL-1 (20 ng icv) elicited fever, suppressed REMS, and increased NREMS for 6 h. NREMS was suppressed for 3 h after the combined intracerebroventricular injections of 5 mg L-NAME and 20 ng IL-1 and was elevated during postinjection hours 4-6. Administration of IL-1 (30 ng/kg iv) increased NREMS and brain temperature for 2 h. After the combined injection of IL-1 and L-NAME (100 mg/kg), NREMS was significantly suppressed during postinjection hours 1-5. It is not known whether the interactions between the sleep-suppressive effects of L-NAME and the NREMS-promoting effects of IL-1 are specific, being mediated via a common mechanism, or whether they are additive, being mediated via independent mechanisms. The pyrogenic and REMS-suppressive actions of either intracerebroventricularly or intravenously injected IL-1 were not affected by L-NAME.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of elevated ambient temperature on sleep, EEG spectra, and brain temperature in the rat

1995 ◽  
Vol 268 (6) ◽  
pp. R1365-R1373 ◽  
Author(s):  
B. O. Gao ◽  
P. Franken ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Ambient Temperature ◽  
Eye Movement ◽  
Spectral Power ◽  
Dark Period ◽  
Brain Temperature ◽  
Spectral Power Density ◽  
State Transitions ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Hypothalamic Temperature

To examine the relationship between sleep and brain temperature in the rat, the vigilance states, spectral power density of the electroencephalogram (EEG), hypothalamic temperature (T(hy)), and cortical temperature (Tcr) were recorded for 3 days. A 1-day rise of ambient temperature from 23 to 30 degrees C did not affect the percentage of waking, non-rapid eye movement sleep (NREMS), and rapid eye movement sleep (REMS), but increased EEG slow-wave activity in NREMS in the 12-h dark period. T(hy) was invariably higher than Tcr, but at 30 degrees C the difference diminished because of a rise in Tcr. In contrast to Tcr, T(hy) was only slightly increased at 30 degrees C and only during sleep and in the dark period. Although the temperatures changed largely in parallel at vigilance state transitions, Tcr rose more rapidly than T(hy) at NREMS-REMS transitions and more slowly at NREMS-waking transitions. T(hy) declined more rapidly than Tcr at waking-NREMS transitions and more slowly at REMS-NREMS transitions. The results are consistent with a central role of the hypothalamus in the activation and deactivation of the waking state.

Epidermal growth factor enhances spontaneous sleep in rabbits

1998 ◽  
Vol 275 (2) ◽  
pp. R509-R514 ◽  
Author(s):  
Tetsuya Kushikata ◽  
Jidong Fang ◽  
Zutang Chen ◽  
Ying Wang ◽  
James M. Krueger
Keyword(s):  
Growth Factors ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Eye Movement ◽  
Brain Temperature ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Guide Cannula ◽  
Epidermal Growth

Several growth factors are implicated in sleep regulation. Epidermal growth factor (EGF) is found in the brain, and it influences the production of several sleep-promoting substances. We determined, therefore, whether administration of exogenous EGF affected spontaneous sleep in rabbits. Twenty-five rabbits were implanted with electroencephalographic electrodes, a brain thermistor, and an intracerebroventricular guide cannula. Three doses of EGF (0.5, 5, and 25 μg) were used. The animals were injected intracerebroventricularly with saline as control and one dose of EGF on 2 separate days. Five and twenty-five micrograms of EGF enhanced non-rapid eye movement sleep and increased brain temperature. The 25-μg dose of EGF also inhibited rapid eye movement sleep across the 23-h postinjection recording period. Results are consistent with the hypothesis that EGF, like other growth factors, could be involved in sleep regulation.

Transient attenuation of CO2 sensitivity after neurotoxic lesions in the medullary raphe area of awake goats

2004 ◽  
Vol 97 (6) ◽  
pp. 2236-2247 ◽  
Author(s):  
M. R. Hodges ◽  
C. Opansky ◽  
B. Qian ◽  
S. Davis ◽  
J. Bonis ◽  
...  
Keyword(s):  
Eye Movement ◽  
Glutamate Receptor ◽  
Tryptophan Hydroxylase ◽  
Ibotenic Acid ◽  
Control Mechanisms ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Medullary Raphe ◽  
Before And After ◽  
Neurokinin 1

The major objective of this study was to gain insight into whether under physiological conditions medullary raphe area neurons influence breathing through CO2/H+ chemoreceptors and/or through a postulated, nonchemoreceptor modulatory influence. Microtubules were chronically implanted into the raphe of adult goats ( n = 13), and breathing at rest (awake and asleep), breathing during exercise, as well as CO2 sensitivity were assessed repeatedly before and after sequential injections of the neurotoxins saporin conjugated to substance P [SP-SAP; neurokinin-1 receptor (NK1R) specific] and ibotenic acid (IA; nonspecific glutamate receptor excitotoxin). In all goats, microtubule implantation alone resulted in altered breathing periods, manifested as central or obstructive apneas, and fractionated breathing. The frequency and characteristics of the altered breathing periods were not subsequently affected by injections of the neurotoxins ( P > 0.05). Three to seven days after SP-SAP or subsequent IA injection, CO2 sensitivity was reduced ( P < 0.05) by 23.8 and 26.8%, respectively, but CO2 sensitivity returned to preinjection control values >7 days postinjection. However, there was no hypoventilation at rest (awake, non-rapid eye movement sleep, or rapid eye movement sleep) or during exercise after these injections ( P > 0.05). The neurotoxin injections resulted in neuronal death greater than three times that with microtubule implantation alone and reduced ( P < 0.05) both tryptophan hydroxylase-expressing (36%) and NK1R-expressing (35%) neurons at the site of injection. We conclude that both NK1R- and glutamate receptor-expressing neurons in the medullary raphe nuclei influence CO2 sensitivity apparently through CO2/H-expressing chemoreception, but the altered breathing periods appear unrelated to CO2 chemoreception and thus are likely due to non-chemoreceptor-related neuromodulation of ventilatory control mechanisms.

scholarly journals Effects of One-Week Tongue-Task Training on Sleep Apnea Severity: A Pilot Study

2015 ◽  
Vol 22 (3) ◽  
pp. 176-178 ◽  
Author(s):  
Eric Rousseau ◽  
César Augusto Melo-Silva ◽  
Simon Gakwaya ◽  
Frédéric Sériès
Keyword(s):  
Sleep Apnea ◽  
Pilot Study ◽  
Randomized Trial ◽  
Eye Movement ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Before And After ◽  
Task Training ◽  
Large Randomized Trial

The aim of the present study was to assess the effects of one-week tongue-task training (TTT) on sleep apnea severity in sleep apnea subjects. Ten patients with sleep apnea (seven men, mean [± SD] age 52±8 years; mean apnea-hypopnea [AHI] index 20.9±5.3 events/h) underwent 1 h TTT in the authors’ laboratory on seven consecutive days. A complete or limited recording and tongue maximal protruding force were assessed before and after one-week TTT. One-week TTT was associated with a global AHI decrease (pre-TTT: 20.9±5.3 events/h; post-TTT: 16.1±5.1 events/h; P<0.001) and AHI decrease during rapid eye movement sleep (pre-TTT: 32.2±18.4 events/h; post-TTT: 16.7±6.6 events/h; P=0.03), while protruding force remained unchanged. The authors consider these results to be potentially clinically relevant and worthy of further investigation in a large randomized trial.

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.

Anti-Ma1– and Anti-Ma2–Associated Encephalitis Manifesting With Rapid Eye Movement Sleep Disorder and Narcolepsy With Cataplexy: A Case Report

2018 ◽  
Vol 83 (5) ◽  
pp. e39-e40 ◽  
Author(s):  
Ilia Kritikou ◽  
Alexandros N. Vgontzas ◽  
Mark A. Rapp ◽  
Edward O. Bixler
Keyword(s):  
Case Report ◽  
Sleep Disorder ◽  
Eye Movement ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep
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