The anterolateral projections of the medial basal hypothalamus affect sleep

The role of the medial basal hypothalamus (MBH) and the anterior hypothalamus/preoptic area (AH/POA) in sleep regulation was investigated using the Halász knife technique to sever MBH anterior and lateral projections in rats. If both lateral and anterior connections of the MBH were cut, rats spent less time in non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS). In contrast, if the lateral connections remained intact, the duration of NREMS and REMS was normal. The diurnal rhythm of NREMS and REMS was altered in all groups except the sham control group. Changes in NREMS or REMS duration were not detected in a group with pituitary stalk lesions. Water consumption was enhanced in three groups of rats, possibly due to the lesion of vasopressin fibers entering the pituitary. EEG delta power during NREMS and brain temperatures (Tbr) were not affected by the cuts during baseline or after sleep deprivation. In response to 4 h of sleep deprivation, only one group, that with the most anterior-to-posterior cuts, failed to increase its NREMS or REMS time during the recovery sleep. After deprivation, Tbr returned to baseline in most of the treatment groups. Collectively, results indicate that the lateral projections of the MBH are important determinants of duration of NREMS and REMS, while more anterior projections are concerned with the diurnal distribution of sleep. Further, the MBH projections involved in sleep regulation are distinct from those involved in EEG delta activity, water intake, and brain temperature.

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Epidermal growth factor enhances spontaneous sleep in rabbits

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1998.275.2.r509 ◽

1998 ◽

Vol 275 (2) ◽

pp. R509-R514 ◽

Cited By ~ 3

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.

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MicroRNA 132 alters sleep and varies with time in brain

Journal of Applied Physiology ◽

10.1152/japplphysiol.00517.2011 ◽

2011 ◽

Vol 111 (3) ◽

pp. 665-672 ◽

Cited By ~ 23

Author(s):

Christopher J. Davis ◽

James M. Clinton ◽

Ping Taishi ◽

Stewart G. Bohnet ◽

Kimberly A. Honn ◽

...

Keyword(s):

Sleep Deprivation ◽

Eye Movement ◽

Dark Period ◽

Wave Activity ◽

Light Period ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Direct Effects ◽

Sleep Regulation ◽

Light Phase

MicroRNA (miRNA) levels in brain are altered by sleep deprivation; however, the direct effects of any miRNA on sleep have not heretofore been described. We report herein that intracerebroventricular application of a miRNA-132 mimetic (preMIR-132) decreased duration of non-rapid-eye-movement sleep (NREMS) while simultaneously increasing duration of rapid eye movement sleep (REMS) during the light phase. Further, preMIR-132 decreased electroencephalographic (EEG) slow-wave activity (SWA) during NREMS, an index of sleep intensity. In separate experiments unilateral supracortical application of preMIR-132 ipsilaterally decreased EEG SWA during NREMS but did not alter global sleep duration. In addition, after ventricular or supracortical injections of preMIR-132, the mimetic-induced effects were state specific, occurring only during NREMS. After local supracortical injections of the mimetic, cortical miRNA-132 levels were higher at the time sleep-related EEG effects were manifest. We also report that spontaneous cortical levels of miRNA-132 were lower at the end of the sleep-dominant light period compared with at the end of the dark period in rats. Results suggest that miRNAs play a regulatory role in sleep and provide a new tool for investigating sleep regulation.

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Interleukin 1 alters rat sleep: temporal and dose-related effects

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1991.260.1.r52 ◽

1991 ◽

Vol 260 (1) ◽

pp. R52-R58 ◽

Cited By ~ 25

Author(s):

M. R. Opp ◽

F. Obal ◽

J. M. Krueger

Keyword(s):

Eye Movement ◽

Slow Wave ◽

Brain Temperature ◽

Interleukin 1 ◽

Wave Activity ◽

Slow Wave Activity ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Sleep Regulation ◽

High Doses

Rats received various doses of interleukin 1 (IL-1) (range, 0.5-25.0 ng) or pyrogen-free saline intracerebroventricularly during the rest (light) and the active (dark) cycles of the day, and sleep-wake activity and brain temperature were determined for 6 h. Low doses of IL-1 (0.5 ng at night, 2.5 ng during the day) increased both the duration of non-rapid-eye-movement sleep (NREMS) and electroencephalogram (EEG) slow-wave activity during NREMS episodes. Increasing doses of IL-1 had divergent effects on NREMS duration and EEG slow-wave activity, and the direction of the changes depended on the diurnal cycle. Thus NREMS duration was promoted at night and EEG slow-wave amplitudes during the day, whereas NREMS duration during the day and EEG slow-wave amplitudes at night were suppressed after higher doses of IL-1. High doses of IL-1 also induced decreases in rapid-eye-movement sleep during both phases of the day. Each dose of IL-1 that promoted NREMS also tended to increase brain temperature. These results demonstrate that IL-1 promotes NREMS in the rat. However, unlike previously reported findings in rabbits, the circadian rhythm of sleep regulation strongly interferes with the sleep-promoting activity of IL-1 in rats.

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The Role of Reproductive Hormones in Sex Differences in Sleep Homeostasis and Arousal Response in Mice

Frontiers in Neuroscience ◽

10.3389/fnins.2021.739236 ◽

2021 ◽

Vol 15 ◽

Author(s):

Jinhwan Choi ◽

Staci J. Kim ◽

Tomoyuki Fujiyama ◽

Chika Miyoshi ◽

Minjeong Park ◽

...

Keyword(s):

Sex Differences ◽

Sleep Deprivation ◽

Eye Movement ◽

Reproductive Hormones ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Sleep Regulation ◽

Male And Female ◽

Sleep Homeostasis ◽

Arousal Response

There are various sex differences in sleep/wake behaviors in mice. However, it is unclear whether there are sex differences in sleep homeostasis and arousal responses and whether gonadal hormones are involved in these sex differences. Here, we examined sleep/wake behaviors under baseline condition, after sleep deprivation by gentle handling, and arousal responses to repeated cage changes in male and female C57BL/6 mice that are hormonally intact, gonadectomized, or gonadectomized with hormone supplementation. Compared to males, females had longer wake time, shorter non-rapid eye movement sleep (NREMS) time, and longer rapid eye movement sleep (REMS) episodes. After sleep deprivation, males showed an increase in NREMS delta power, NREMS time, and REMS time, but females showed a smaller increase. Females and males showed similar arousal responses. Gonadectomy had only a modest effect on homeostatic sleep regulation in males but enhanced it in females. Gonadectomy weakened arousal response in males and females. With hormone replacement, baseline sleep in gonadectomized females was similar to that of intact females, and baseline sleep in gonadectomized males was close to that of intact males. Gonadal hormone supplementation restored arousal response in males but not in females. These results indicate that male and female mice differ in their baseline sleep–wake behavior, homeostatic sleep regulation, and arousal responses to external stimuli, which are differentially affected by reproductive hormones.

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Growth hormone-releasing hormone and corticotropin-releasing hormone enhance non-rapid-eye-movement sleep after sleep deprivation

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00641.2005 ◽

2006 ◽

Vol 291 (3) ◽

pp. E549-E556 ◽

Cited By ~ 25

Author(s):

P. Schüssler ◽

A. Yassouridis ◽

M. Uhr ◽

M. Kluge ◽

J. Weikel ◽

...

Keyword(s):

Growth Hormone ◽

Sleep Deprivation ◽

Eye Movement ◽

Hormone Secretion ◽

Rapid Eye Movement ◽

Rapid Eye Movement Sleep ◽

Corticotropin Releasing Hormone ◽

Endocrine Activity ◽

Releasing Hormone ◽

Recovery Sleep

The neuropeptides growth hormone (GH)-releasing hormone (GHRH) and corticotropin-releasing hormone (CRH) regulate sleep and nocturnal hormone secretion in a reciprocal fashion, at least in males. GHRH promotes sleep and GH and inhibits hypothalamo-pituitary-adrenocortical (HPA) hormones. CRH exerts opposite effects. In women, a sexual dimorphism was found because GHRH impairs sleep and stimulates HPA hormones. Sleep deprivation (SD) is the most powerful stimulus for inducing sleep. Studies in rodents show a key role of GHRH in sleep promotion after SD. The effects of GHRH and CRH on sleep-endocrine activity during the recovery night after SD are unknown. We compared sleep EEG, GH, and cortisol secretion between nights before and after 40 h of SD in 48 normal women and men aged 19–67 yr. During the recovery night, GHRH, CRH, or placebo were injected repetitively. After placebo during the recovery night, non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS) increased and wakefulness decreased compared with the baseline night. After GHRH, the increase of NREMS and the decrease of wakefulness were more distinct than after placebo. Also, after CRH, NREMS increased higher than after placebo, and a positive correlation was found between age and the baseline-related increase of slow-wave sleep. REMS increased after placebo and after GHRH, but not after CRH. EEG spectral analysis showed increases in the lower frequencies and decreases in the higher frequencies during NREMS after each of the treatments. Cortisol and GH did not differ between baseline and recovery nights after placebo. After GHRH, GH increased and cortisol decreased. Cortisol increased after CRH. No sex differences were found in these changes. Our data suggest that GHRH and CRH augment NREMS promotion after SD. Marked differences appear to exist in peptidergic sleep regulation between spontaneous and recovery sleep.

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