Sleep of transgenic mice producing excess rat growth hormone

2002 ◽  
Vol 282 (1) ◽  
pp. R70-R76 ◽  
Author(s):  
I. Hajdu ◽  
F. Obal ◽  
J. Fang ◽  
J. M. Krueger ◽  
C. D. Rollo
Keyword(s):  
Growth Hormone ◽  
Transgenic Mice ◽  
Eye Movement ◽  
Hormonal Changes ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Rat Growth ◽  
Electroencephalogram Eeg

The effects of chronic excess of growth hormone (GH) on sleep-wake activity was determined in giant transgenic mice in which the metallothionein-1 promoter stimulates the expression of rat GH (MT-rGH mice) and in their normal littermates. In the MT-rGH mice, the time spent in spontaneous non-rapid eye movement sleep (NREMS) was enhanced moderately, and rapid eye movement sleep (REMS) time increased greatly during the light period. After a 12-h sleep deprivation, the MT-rGH mice continued to sleep more than the normal mice, but there were no differences in the increments in NREMS, REMS, and electroencephalogram (EEG) slow-wave activity (SWA) during NREMS between the two groups. Injection of the somatostatin analog octreotide elicited a prompt sleep suppression followed by increases in SWA during NREMS in normal mice. These changes were attenuated in the MT-rGH mice. The decreased responsiveness to octreotide is explained by a chronic suppression of hypothalamic GH-releasing hormone in the MT-rGH mice. Enhancements in spontaneous REMS are attributed to the REMS-promoting activity of GH. The increases in spontaneous NREMS are, however, not consistent with our current understanding of the role of somatotropic hormones in sleep regulation. Metabolic, neurotransmitter, or hormonal changes associated with chronic GH excess may indirectly influence sleep.

Growth hormone-releasing hormone: cerebral cortical sleep-related EEG actions and expression

2007 ◽  
Vol 293 (2) ◽  
pp. R922-R930 ◽  
Author(s):  
Éva Szentirmai ◽  
Tadanobu Yasuda ◽  
Ping Taishi ◽  
Mingxiang Wang ◽  
Lynn Churchill ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Eye Movement ◽  
Wave Power ◽  
Growth Hormone Releasing Hormone ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Delta Wave ◽  
Releasing Hormone ◽  
Delta Power

Growth hormone-releasing hormone (GHRH), its receptor (GHRHR), and other members of the somatotropic axis are involved in non-rapid eye movement sleep (NREMS) regulation. Previously, studies established the involvement of hypothalamic GHRHergic mechanisms in NREMS regulation, but cerebral cortical GHRH mechanisms in sleep regulation remained uninvestigated. Here, we show that unilateral application of low doses of GHRH to the surface of the rat somatosensory cortex ipsilaterally decreased EEG delta wave power, while higher doses enhanced delta power. These actions of GHRH on EEG delta wave power occurred during NREMS but not during rapid eye movement sleep. Further, the cortical forms of GHRH and GHRHR were identical to those found in the hypothalamus and pituitary, respectively. Cortical GHRHR mRNA and protein levels did not vary across the day-night cycle, whereas cortical GHRH mRNA increased with sleep deprivation. These results suggest that cortical GHRH and GHRHR have a role in the regulation of localized EEG delta power that is state dependent, as well as in their more classic hypothalamic role in NREMS regulation.

Spontaneous sleep and homeostatic sleep regulation in ghrelin knockout mice

2007 ◽  
Vol 293 (1) ◽  
pp. R510-R517 ◽  
Author(s):  
Éva Szentirmai ◽  
Levente Kapás ◽  
Yuxiang Sun ◽  
Roy G. Smith ◽  
James M. Krueger
Keyword(s):  
Eye Movement ◽  
Diurnal Rhythms ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Compensatory Mechanisms ◽  
Regulatory Circuit ◽  
Normal Sleep ◽  
The Brain

Ghrelin is well known for its feeding and growth hormone-releasing actions. It may also be involved in sleep regulation; intracerebroventricular administration and hypothalamic microinjections of ghrelin stimulate wakefulness in rats. Hypothalamic ghrelin, together with neuropeptide Y and orexin form a food intake-regulatory circuit. We hypothesized that this circuit also promotes arousal. To further investigate the role of ghrelin in the regulation of sleep-wakefulness, we characterized spontaneous and homeostatic sleep regulation in ghrelin knockout (KO) and wild-type (WT) mice. Both groups of mice exhibited similar diurnal rhythms with more sleep and less wakefulness during the light period. In ghrelin KO mice, spontaneous wakefulness and rapid-eye-movement sleep (REMS) were slightly elevated, and non-rapid-eye-movement sleep (NREMS) was reduced. KO mice had more fragmented NREMS than WT mice, as indicated by the shorter and greater number of NREMS episodes. Six hours of sleep deprivation induced rebound increases in NREMS and REMS and biphasic changes in electroencephalographic slow-wave activity (EEG SWA) in both genotypes. Ghrelin KO mice recovered from NREMS and REMS loss faster, and the delayed reduction in EEG SWA, occurring after sleep loss-enhanced increases in EEG SWA, was shorter-lasting compared with WT mice. These findings suggest that the basic sleep-wake regulatory mechanisms in ghrelin KO mice are not impaired and they are able to mount adequate rebound sleep in response to a homeostatic challenge. It is possible that redundancy in the arousal systems of the brain or activation of compensatory mechanisms during development allow for normal sleep-wake regulation in ghrelin KO mice.

GABAergic Neurons in the Dorsal–Intermediate Lateral Septum Regulate Sleep–Wakefulness and Anesthesia in Mice

2021 ◽  
Author(s):  
Di Wang ◽  
Qingchen Guo ◽  
Yu Zhou ◽  
Zheng Xu ◽  
Su-Wan Hu ◽  
...  
Keyword(s):  
General Anesthesia ◽  
Eye Movement ◽  
Gabaergic Neurons ◽  
Lateral Septum ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Awake State ◽  
Isoflurane Anesthesia

Background The γ-aminobutyric acid–mediated (GABAergic) inhibitory system in the brain is critical for regulation of sleep–wake and general anesthesia. The lateral septum contains mainly GABAergic neurons, being cytoarchitectonically divided into the dorsal, intermediate, and ventral parts. This study hypothesized that GABAergic neurons of the lateral septum participate in the control of wakefulness and promote recovery from anesthesia. Methods By employing fiber photometry, chemogenetic and optogenetic neuronal manipulations, anterograde tracing, in vivo electrophysiology, and electroencephalogram/electromyography recordings in adult male mice, the authors measured the role of lateral septum GABAergic neurons to the control of sleep–wake transition and anesthesia emergence and the corresponding neuron circuits in arousal and emergence control. Results The GABAergic neurons of the lateral septum exhibited high activities during the awake state by in vivo fiber photometry recordings (awake vs. non–rapid eye movement sleep: 3.3 ± 1.4% vs. –1.3 ± 1.2%, P < 0.001, n = 7 mice/group; awake vs. anesthesia: 2.6 ± 1.2% vs. –1.3 ± 0.8%, P < 0.001, n = 7 mice/group). Using chemogenetic stimulation of lateral septum GABAergic neurons resulted in a 100.5% increase in wakefulness and a 51.2% reduction in non–rapid eye movement sleep. Optogenetic activation of these GABAergic neurons promoted wakefulness from sleep (median [25th, 75th percentiles]: 153.0 [115.9, 179.7] s to 4.0 [3.4, 4.6] s, P = 0.009, n = 5 mice/group) and accelerated emergence from isoflurane anesthesia (514.4 ± 122.2 s vs. 226.5 ± 53.3 s, P < 0.001, n = 8 mice/group). Furthermore, the authors demonstrated that the lateral septum GABAergic neurons send 70.7% (228 of 323 cells) of monosynaptic projections to the ventral tegmental area GABAergic neurons, preferentially inhibiting their activities and thus regulating wakefulness and isoflurane anesthesia depth. Conclusions The results uncover a fundamental role of the lateral septum GABAergic neurons and their circuit in maintaining awake state and promoting general anesthesia emergence time. Editor’s Perspective What We Already Know about This Topic What This Article Tells Us That Is New

Normal EEG in Wakefulness and Sleep

2017 ◽  
Author(s):  
Vaishnav Krishnan ◽  
Bernard S. Chang ◽  
Donald L. Schomer
Keyword(s):  
Eye Movement ◽  
Low Voltage ◽  
Theta Activity ◽  
Normal Adult ◽  
Alpha Band ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Delta Activity ◽  
Electroencephalogram Eeg

The normal adult electroencephalogram (EEG) is not a singular entity, and recognizing and appreciating the various expressions of a normal EEG is vital for any electroencephalographer. During wakefulness, the posterior dominant rhythm (PDR) must display a frequency within the alpha band, although an absent PDR is not abnormal. A symmetrically slowed PDR, excessive theta activity, or any delta activity during wakefulness is abnormal and a biomarker of encephalopathy. Low-voltage EEGs have been associated with a variety of neuropathological states but are themselves not abnormal. During non-rapid eye movement sleep, a normal EEG will display progressively greater degrees of background slowing and amplitude enhancement, which may or may not be associated with specific sleep-related transients. In contrast, the EEG during rapid eye movement sleep more closely resembles a waking EEG (“desynchronized”) in amplitude and background frequencies. Across both wakefulness and sleep, significant asymmetries in background frequencies and amplitude are abnormal.

scholarly journals Dream Recall upon Awakening from Non-Rapid Eye Movement Sleep in Older Adults: Electrophysiological Pattern and Qualitative Features

2020 ◽  
Vol 10 (6) ◽  
pp. 343 ◽  
Author(s):  
Serena Scarpelli ◽  
Aurora D’Atri ◽  
Chiara Bartolacci ◽  
Maurizio Gorgoni ◽  
Anastasia Mangiaruga ◽  
...  
Keyword(s):  
Eye Movement ◽  
Sleep Stage ◽  
Nrem Sleep ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Dream Recall ◽  
Cortical Arousal ◽  
Beta Power ◽  
Dream Report

Several findings support the activation hypothesis, positing that cortical arousal promotes dream recall (DR). However, most studies have been carried out on young participants, while the electrophysiological (EEG) correlates of DR in older people are still mostly unknown. We aimed to test the activation hypothesis on 20 elders, focusing on the Non-Rapid Eye Movement (NREM) sleep stage. All the subjects underwent polysomnography, and a dream report was collected upon their awakening from NREM sleep. Nine subjects were recallers (RECs) and 11 were non-RECs (NRECs). The delta and beta EEG activity of the last 5 min and the total NREM sleep was calculated by Fast Fourier Transform. Statistical comparisons (RECs vs. NRECs) revealed no differences in the last 5 min of sleep. Significant differences were found in the total NREM sleep: the RECs showed lower delta power over the parietal areas than the NRECs. Consistently, statistical comparisons on the activation index (delta/beta power) revealed that RECs showed a higher level of arousal in the fronto-temporal and parieto-occipital regions than NRECs. Both visual vividness and dream length are positively related to the level of activation. Overall, our results are consistent with the view that dreaming and the storage of oneiric contents depend on the level of arousal during sleep, highlighting a crucial role of the temporo-parietal-occipital zone.

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