Zebrafish as a tool in the study of sleep and memory-related disorders

2021 ◽  
Vol 19 ◽  
Author(s):  
Stefani Altenhofen ◽  
Carla Denise Bonan
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Sleep State ◽  
Brain Wave ◽  
Synaptic Homeostasis ◽  
Brain Wave Activity

: Sleep is an evolutionarily conserved phenomenon, being an essential biological necessity for the learning process and memory consolidation. The brain displays two types of electrical activity during sleep: slow-wave activity or non-rapid eye movement (NREM) sleep and desynchronized brain wave activity or rapid eye movement (REM) sleep. There are many theories about “Why we need to sleep?” among them the synaptic homeostasis. This theory proposes that the role of sleep is the restoration of synaptic homeostasis, which is destabilized by synaptic strengthening triggered by learning during waking and by synaptogenesis during development. Sleep diminishes the plasticity load on neurons and other cells to normalize synaptic strength. In contrast, it re-establishes neuronal selectivity and the ability to learn, leading to the consolidation and integration of memories. The use of zebrafish as a tool to assess sleep and its disorders is growing, although sleep in this animal is not yet divided, for example, into REM and NREM states. However, zebrafish are known to have a regulated daytime circadian rhythm. Their sleep state is characterized by periods of inactivity accompanied by an increase in arousal threshold, preference for resting place, and the “rebound sleep effect” phenomenon, which causes an increased slow-wave activity after a forced waking period. In addition, drugs known to modulate sleep, such as melatonin, nootropics, and nicotine, have been tested in zebrafish. In this review, we discuss the use of zebrafish as a model to investigate sleep mechanisms and their regulation, demonstrating this species as a promising model for sleep research.

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.

Electroencephalogram analysis of non-rapid eye movement sleep in rats

1988 ◽  
Vol 255 (1) ◽  
pp. R27-R37 ◽  
Author(s):  
L. Trachsel ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Power Spectra ◽  
Low Frequency ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Episode Duration ◽  
High Frequency Activity

Sleep states and power spectra of the electroencephalogram were determined for consecutive 4-s epochs during 24 h in rats that had been implanted with electrodes under deep pentobarbital anesthesia. The power spectra in non-rapid eye movement sleep (NREMS) showed marked trends: low-frequency activity (0.75-7.0 Hz) declined progressively throughout the 12-h light period (L) and remained low during most of the 12-h dark period (D); high-frequency activity (10.25-25.0 Hz) rose toward the end of L and reached a maximum at the beginning of D. Within a single NREMS episode (duration 0.5-5.0 min), slow-wave activity (0.75-4.0 Hz) increased progressively to a plateau level. The rise was approximated by a saturating exponential function: although the asymptote level of the function showed a prominent 24-h rhythm, the time constant remained relatively stable (approximately 40 s). After short interruptions of NREMS episodes, slow-wave activity rose more steeply than after long interruptions. The marked 24-h variation of maximum slow-wave activity within NREMS episodes may reflect the level of a homeostatic sleep process.

Varying photoperiod in the laboratory rat: profound effect on 24-h sleep pattern but no effect on sleep homeostasis

1995 ◽  
Vol 269 (3) ◽  
pp. R691-R701 ◽  
Author(s):  
P. Franken ◽  
I. Tobler ◽  
A. A. Borbely
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Sleep Pattern ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Sleep Regulation ◽  
Marked Rise ◽  
Laboratory Rats

To assess the influence of the photoperiod on sleep regulation, laboratory rats were adapted to a long photoperiod (LPP; 16:8-h light-dark cycle, LD 16:8) or a short photoperiod (SPP; LD 8:16). The electroencephalogram (EEG) and cortical temperature (TCRT) were continuously recorded for a baseline day, a 24-h sleep deprivation (SD) period, and a recovery day. Data obtained previously for LD 12:12 served for comparison. Whereas the photoperiod exerted a prominent effect on the 24-h sleep pattern, the 24-h baseline level of sleep and the response to SD were little affected. Recovery from SD was characterized by a marked rise in rapid eye movement sleep, a moderate rise in non-rapid eye movement sleep, and an initial enhancement of EEG slow-wave activity followed by a decrease below baseline. The amplitude and phase of the "unmasked" 24-h component of TCRT did not differ between LPP and SPP. Computer simulations demonstrated that the changes of TCRT and EEG slow-wave activity can be largely accounted for by the sequence of the vigilance states. We conclude that the photoperiod does not affect the basic processes underlying sleep regulation.

scholarly journals The role of non-rapid eye movement slow-wave activity in prefrontal metabolism across young and middle-aged adults

2016 ◽  
Vol 25 (3) ◽  
pp. 296-306 ◽  
Author(s):  
Kristine A. Wilckens ◽  
Howard J. Aizenstein ◽  
Eric A. Nofzinger ◽  
Jeffrey A. James ◽  
Brant P. Hasler ◽  
...  
Keyword(s):  
Eye Movement ◽  
Slow Wave ◽  
Wave Activity ◽  
Slow Wave Activity ◽  
Rapid Eye Movement ◽  
Middle Aged ◽  
Middle Aged Adults

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 Visual imagery and visual perception induce similar changes in occipital slow waves of sleep

2019 ◽  
Vol 121 (6) ◽  
pp. 2140-2152 ◽  
Author(s):  
Giulio Bernardi ◽  
Monica Betta ◽  
Jacinthe Cataldi ◽  
Andrea Leo ◽  
José Haba-Rubio ◽  
...  
Keyword(s):  
Visual Perception ◽  
Eye Movement ◽  
Slow Wave ◽  
Visual Imagery ◽  
Nrem Sleep ◽  
Wave Activity ◽  
Slow Waves ◽  
Slow Wave Activity ◽  
Short Term ◽  
Visual Areas

Previous studies have shown that regional slow-wave activity (SWA) during non-rapid eye movement (NREM) sleep is modulated by prior experience and learning. Although this effect has been convincingly demonstrated for the sensorimotor domain, attempts to extend these findings to the visual system have provided mixed results. In this study we asked whether depriving subjects of external visual stimuli during daytime would lead to regional changes in slow waves during sleep and whether the degree of “internal visual stimulation” (spontaneous imagery) would influence such changes. In two 8-h sessions spaced 1 wk apart, 12 healthy volunteers either were blindfolded while listening to audiobooks or watched movies (control condition), after which their sleep was recorded with high-density EEG. We found that during NREM sleep, the number of small, local slow waves in the occipital cortex decreased after listening with blindfolding relative to movie watching in a way that depended on the degree of visual imagery subjects reported during blindfolding: subjects with low visual imagery showed a significant reduction of occipital sleep slow waves, whereas those who reported a high degree of visual imagery did not. We also found a positive relationship between the reliance on visual imagery during blindfolding and audiobook listening and the degree of correlation in sleep SWA between visual areas and language-related areas. These preliminary results demonstrate that short-term alterations in visual experience may trigger slow-wave changes in cortical visual areas. Furthermore, they suggest that plasticity-related EEG changes during sleep may reflect externally induced (“bottom up”) visual experiences, as well as internally generated (“top down”) processes.NEW & NOTEWORTHY Previous work has shown that slow-wave activity, a marker of sleep depth, is linked to neural plasticity in the sensorimotor cortex. We show that after short-term visual deprivation, subjects who reported little visual imagery had a reduced incidence of occipital slow waves. This effect was absent in subjects who reported strong spontaneous visual imagery. These findings suggest that visual imagery may “substitute” for visual perception and induce similar changes in non-rapid eye movement slow waves.

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