Persistence of sleep-temperature coupling after suprachiasmatic nuclei lesions in rats

The suprachiasmatic nucleus (SCN) regulates the circadian rhythms of body temperature (Tb) and vigilance states in mammals. We studied rats in which circadian rhythmicity was abolished after SCN lesions (SCNx rats) to investigate the association between the ultradian rhythms of sleep-wake states and brain temperature (Tbr), which are exposed after lesions. Ultradian rhythms of Tbr (mean period: 3.6 h) and sleep were closely associated in SCNx rats. Within each ultradian cycle, nonrapid eye movement (NREM) sleep was initiated 5 ± 1 min after Tbr peaks, after which temperature continued a slow decline (0.02 ± 0.006°C/min) until it reached a minimum. Sleep and slow wave activity (SWA), an index of sleep intensity, were associated with declining temperature. Cross-correlation analysis revealed that the rhythm of Tbr preceded that of SWA by 2–10 min. We also investigated the thermoregulatory and sleep-wake responses of SCNx rats and controls to mild ambient cooling (18°C) and warming (30°C) over 24-h periods. SCNx rats and controls responded similarly to changes in ambient temperature. Cooling decreased REM sleep and increased wake. Warming increased Tbr, blunted the amplitude of ultradian Tbr rhythms, and increased the number of transitions into NREM sleep. SCNx rats and controls had similar percentages of NREM sleep, REM sleep, and wake, as well as the same average Tb within each 24-h period. Our results suggest that, in rats, the SCN modulates the timing but not the amount of sleep or the homeostatic control of sleep-wake states or Tb during deviations in ambient temperature.

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Loss of circadian organization of sleep and wakefulness during hibernation

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00771.2000 ◽

2002 ◽

Vol 282 (4) ◽

pp. R1086-R1095 ◽

Cited By ~ 22

Author(s):

Jennie E. Larkin ◽

Paul Franken ◽

H. Craig Heller

Keyword(s):

Brain Temperature ◽

Nrem Sleep ◽

Wave Activity ◽

Ground Squirrels ◽

Ultradian Rhythm ◽

Organization Of Sleep ◽

Sleep Homeostasis ◽

Circadian Organization ◽

Frequency Components ◽

Torpor Bouts

We investigated circadian and homeostatic regulation of nonrapid eye movement (NREM) sleep in golden-mantled ground squirrels during euthermic intervals between torpor bouts. Slow-wave activity (SWA; 1–4 Hz) and sigma activity (10–15 Hz) represent the two dominant electroencephalographic (EEG) frequency components of NREM sleep. EEG sigma activity has a strong circadian component in addition to a sleep homeostatic component, whereas SWA mainly reflects sleep homeostasis [Dijk DJ and Czeisler CA. J Neurosci 15: 3526–3538, 1995; Dijk DJ, Shanahan TL, Duffy JF, Ronda JM, and Czeisler CA. J Physiol (Lond) 505: 851–858, 1997]. Animals maintained under constant conditions continued to display circadian rhythms in both sigma activity and brain temperature throughout euthermic intervals, whereas sleep and wakefulness showed no circadian organization. Instead, sleep and wakefulness were distributed according to a 6-h ultradian rhythm. SWA, NREM sleep bout length, and sigma activity responded homeostatically to the ultradian sleep-wake pattern. We suggest that the loss of sleep-wake consolidation in ground squirrels during the hibernation season may be related to the greatly decreased locomotor activity during the hibernation season and may be necessary for maintenance of multiday torpor bouts characteristic of hibernating species.

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Hypocretin in locus coeruleus and dorsal raphe nucleus mediates inescapable footshock stimulation (IFS)-induced REM sleep alteration

SLEEP ◽

10.1093/sleep/zsab301 ◽

2021 ◽

Author(s):

Yun Lo ◽

Pei-Lu Yi ◽

Yi-Tse Hsiao ◽

Fang-Chia Chang

Keyword(s):

Locus Coeruleus ◽

Rem Sleep ◽

Energy Homeostasis ◽

Dorsal Raphe Nucleus ◽

Nrem Sleep ◽

Dorsal Raphe ◽

Wave Activity ◽

Raphe Nucleus ◽

Sleep Disruption ◽

Dorsal Raphé

Abstract Hypocretin (hcrt) is a stress-reacting neuropeptide mediating arousal and energy homeostasis. An inescapable footshock stimulation (IFS) could initiate the hcrt release from the lateral hypothalamus (LHA) and suppresses rapid eye movement (REM) sleep in rodents. However, the effects of the IFS-induced hcrts on REM-off nuclei, the locus coeruleus (LC) and dorsal raphe nucleus (DRN), remained unclear. We hypothesized that the hcrt projections from the LHA to LC or DRN mediate IFS-induced sleep disruption. Our results demonstrated that the IFS increased hcrt expression and the neuronal activities in the LHA, hypothalamus, brainstem, thalamus, and amygdala. Suppressions of REM sleep and slow wave activity during non-REM (NREM) sleep caused by the high expression of hcrts were blocked when a non-specific and dual hcrt receptor antagonist was administered into the LC or DRN. Furthermore, the IFS also caused an elevated innate anxiety, but was limitedly influenced by the hcrt antagonist. This result suggests that the increased hcrt concentrations in the LC and DRN mediate stress-induced sleep disruptions and might partially involve IFS-induced anxiety.

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Natural hypothermia and sleep deprivation: common effects on recovery sleep in the Djungarian hamster

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1996.271.5.r1364 ◽

1996 ◽

Vol 271 (5) ◽

pp. R1364-R1371 ◽

Cited By ~ 6

Author(s):

T. Deboer ◽

I. Tobler

Keyword(s):

Sleep Deprivation ◽

Brain Temperature ◽

Alternative Hypothesis ◽

Nrem Sleep ◽

Wave Activity ◽

Daily Torpor ◽

Djungarian Hamster ◽

Subsequent Increase ◽

Recovery Sleep ◽

Sleep Debt

Sleep, daily torpor, and hibernation have been considered to be homologous processes. However, in the Djungarian hamster, daily torpor is followed by an increase in slow-wave activity (SWA; electroencephalogram power density 0.75-4.0 Hz) that is similar to the increase observed after sleep deprivation. A positive correlation was found between torpor episode length and the subsequent increase in SWA, which was highest when SWA was assumed to increase with a saturating exponential function. Thus the increase in SWA propensity during daily torpor followed similar kinetics as during waking, supporting the hypothesis that when the animal is in torpor it is incurring a sleep debt. An alternative hypothesis, proposing that the mode of arousal causes the subsequent SWA increase, was tested by warming the animals during emergence from daily torpor. Irrespective of mode of arousal, more non-rapid eye movement (NREM) sleep and a similar SWA increase was found after torpor. The data are compatible with a putative neuronal restorative function for sleep associated with the expression of SWA in NREM sleep. During torpor, when brain temperature is low, this function is inhibited, whereas the need for restoration accumulates. Recovery takes place only after return to euthermia.

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An ether stressor increases REM sleep in rats: possible role of prolactin

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.2000.279.5.r1590 ◽

2000 ◽

Vol 279 (5) ◽

pp. R1590-R1598 ◽

Cited By ~ 27

Author(s):

B. Bodosi ◽

F. Obál ◽

J. Gardi ◽

J. Komlódi ◽

J. Fang ◽

...

Keyword(s):

Eye Movement ◽

Rem Sleep ◽

Nrem Sleep ◽

Wave Activity ◽

Intracerebroventricular Administration ◽

Light Onset ◽

Hypophysectomized Rats ◽

Sleep Alterations ◽

Stimulation Of

Sleep alterations after a 1-min exposure to ether vapor were studied in rats to determine if this stressor increases rapid eye-movement (REM) sleep as does an immobilization stressor. Ether exposure before light onset or dark onset was followed by significant increases in REM sleep starting ∼3–4 h later and lasting for several hours. Non-REM (NREM) sleep and electroencephalographic slow-wave activity during NREM sleep were not altered. Exposure to ether vapor elicited prolactin (Prl) secretion. REM sleep was not promoted after ether exposure in hypophysectomized rats. If the hypophysectomy was partial and the rats secreted Prl after ether exposure, then increases in REM sleep were observed. Intracerebroventricular administration of an antiserum to Prl decreased spontaneous REM sleep and inhibited ether exposure-induced REM sleep. The results indicate that a brief exposure to ether vapor is followed by increases in REM sleep if the Prl response associated with stress is unimpaired. This suggests that Prl, which is a previously documented REM sleep-promoting hormone, may contribute to the stimulation of REM sleep after ether exposure.

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Narcolepsy and the Dissociation of REM Sleep and Cataplexy through Ambient Temperature Manipulation

10.1101/2021.12.29.474449 ◽

2021 ◽

Author(s):

Bianca Viberti ◽

Lisa Branca ◽

Simone Bellini ◽

Claudio LA Bassetti ◽

Antoine Adamantidis ◽

...

Keyword(s):

Ambient Temperature ◽

Rem Sleep ◽

Activity Patterns ◽

Active Phase ◽

Nrem Sleep ◽

Dark Phase ◽

Inactive Phase ◽

Temperature Manipulation ◽

Unexpected Findings ◽

Sleep Propensity

Narcolepsy is characterized by increased REM sleep propensity and cataplexy. Although narcolepsy is caused by the selective loss or dysfunction of hypocretin (Hcrt) neurons within the lateral hypothalamus (LH), mechanisms underlying REM sleep propensity and cataplexy remain to be elucidated. We have recently shown that wild type (WT) mice increase REM sleep expression when exposed to thermoneutral ambient temperature (Ta) warming during the light (inactive) phase. We hypothesized that the loss of Hcrt may lead to exaggerated responses with respect to increased REM sleep and cataplexy during Ta warming. To test this hypothesis, Hcrt-KO mice were implanted for chronic sleep recordings and housed in a temperature-controlled cabinet. Sleep-wake expression and both spontaneous cataplexy and food-elicited cataplexy were evaluated at constant Ta and during a Ta manipulation protocol. Here we show several unexpected findings. First, Hcrt-KO mice show opposite circadian patterns with respect to REM sleep responsiveness to thermoneutral Ta warming compared to WT mice. As previously demonstrated, WT mice increased REM sleep when Ta warming is presented during the inactive (light) phase, whereas Hcrt-KO showed a significant decrease in REM sleep expression. In contrast, Hcrt-KO mice increased REM sleep expression upon exposure to Ta warming when presented during the active (dark) phase, a circadian time when WT mice showed no significant changes in REM sleep as a function of Ta. Second, we found that REM sleep and cataplexy can be dissociated through Ta manipulation. Specifically, although Ta warming significantly increased REM sleep expression in Hcrt-KO mice during the active phase, cataplexy bout number and total cataplexy duration significantly decreased. In contrast, cataplexy expression was favoured during Ta cooling when REM sleep expression significantly decreased. Finally, video actigraphy and sleep-wake recordings in Hcrt-KO mice demonstrated that Ta manipulation did not significantly alter waking motor activity patterns or waking or NREM sleep durations. These data suggest that neural circuits gating REM sleep and cataplexy expression can be dissociated with Ta manipulation.

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