Protocol for Drosophila sleep deprivation using single-chip board.
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ABSTRACT:
SUBMITTER: Jin X
PROVIDER: S-EPMC8456114 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Sleep disturbances negatively impact numerous functions and have been linked to aggression and violence. However, a clear effect of sleep deprivation on aggressive behaviors remains unclear. We find that acute sleep deprivation profoundly suppresses aggressive behaviors in the fruit fly, while other social behaviors are unaffected. This suppression is recovered following post-deprivation sleep rebound, and occurs regardless of the approach to achieve sleep loss. Genetic and pharmacologic approaches suggest octopamine signaling transmits changes in aggression upon sleep deprivation, and reduced aggression places sleep-deprived flies at a competitive disadvantage for obtaining a reproductive partner. These findings demonstrate an interaction between two phylogenetically conserved behaviors, and suggest that previous sleep experiences strongly modulate aggression with consequences for reproductive fitness.
| S-EPMC4515473 | biostudies-literature
Project description:Study objectivesSleep rebound-the increase in sleep that follows sleep deprivation-is a hallmark of homeostatic sleep regulation that is conserved across the animal kingdom. However, both the mechanisms that underlie sleep rebound and its relationship to habitual daily sleep remain unclear. To address this, we developed an efficient thermogenetic method of inducing sleep deprivation in Drosophila that produces a substantial rebound, and applied the newly developed method to assess sleep rebound in a screen of 1,741 mutated lines. We used data generated by this screen to identify lines with reduced sleep rebound following thermogenetic sleep deprivation, and to probe the relationship between habitual sleep amount and sleep following thermogenetic sleep deprivation in Drosophila.MethodsTo develop a thermogenetic method of sleep deprivation suitable for screening, we thermogenetically stimulated different populations of wake-promoting neurons labeled by Gal4 drivers. Sleep rebound following thermogenetically-induced wakefulness varies across the different sets of wake-promoting neurons that were stimulated, from very little to quite substantial. Thermogenetic activation of neurons marked by the c584-Gal4 driver produces both strong sleep loss and a substantial rebound that is more consistent within genotypes than rebound following mechanical or caffeine-induced sleep deprivation. We therefore used this driver to induce sleep deprivation in a screen of 1,741 mutagenized lines generated by the Drosophila Gene Disruption Project. Flies were subjected to 9 h of sleep deprivation during the dark period and released from sleep deprivation 3 h before lights-on. Recovery was measured over the 15 h following sleep deprivation. Following identification of lines with reduced sleep rebound, we characterized baseline sleep and sleep depth before and after sleep deprivation for these hits.ResultsWe identified two lines that consistently exhibit a blunted increase in the duration and depth of sleep after thermogenetic sleep deprivation. Neither of the two genotypes has reduced total baseline sleep. Statistical analysis across all screened lines shows that genotype is a strong predictor of recovery sleep, independent from effects of genotype on baseline sleep.ConclusionsOur data show that rebound sleep following thermogenetic sleep deprivation can be genetically separated from sleep at baseline. This suggests that genetically controlled mechanisms of sleep regulation not manifest under undisturbed conditions contribute to sleep rebound following thermogenetic sleep deprivation.
| S-EPMC4835307 | biostudies-literature
Project description:Exploration of deep space poses many challenges. Mission support personnel will not be immediately available to assist crewmembers performing complex operations on future long-duration exploration operations. Consequently, it is imperative that crewmembers have objective, reliable, and non-invasive metrics available to aid them in determining their fitness for duty prior to engaging in potentially dangerous tasks. The Robotics On-Board Trainer (ROBoT) task is NASA's platform for training astronauts to perform docking and grappling maneuvers. It is regularly used by crewmembers during spaceflight for refresher training. The operational ROBoT system, however, does not record data. Thus, a research version of ROBoT, called ROBoT-r, was developed so that operationally relevant data could be mined to provide feedback to crewmembers. We investigated whether ROBoT-r metrics would change according to sleep loss and circadian phase in a 28-h laboratory-based sleep deprivation study. Overall, participants showed improvement over time despite sleep loss, indicating continued learning. Performance on the psychomotor vigilance task (PVT) followed an expected profile, with reduced performance across the night. These findings suggest that individuals may be able to temporarily compensate for sleep loss to maintain performance on complex, novel tasks. It is possible that some ROBoT-r metrics may be sensitive to sleep loss after longer bouts of wakefulness or after individuals have habituated to the task. Studies with additional participants and extended pre-training on the ROBoT-r task should be conducted to disentangle how brain activity may change as individuals learn and habituate to complex tasks during sleep loss.
| S-EPMC7385239 | biostudies-literature
Project description:The role of the transmembrane receptor Notch in the adult brain is poorly understood. Here, we provide evidence that bunched, a negative regulator of Notch, is involved in sleep homeostasis. Genetic evidence indicates that interfering with bunched activity in the mushroom bodies (MBs) abolishes sleep homeostasis. Combining bunched and Delta loss-of-function mutations rescues normal homeostasis, suggesting that Notch signaling may be involved in regulating sensitivity to sleep loss. Preventing the downregulation of Delta by overexpressing a wild-type transgene in MBs reduces sleep homeostasis and, importantly, prevents learning impairments induced by sleep deprivation. Similar resistance to sleep loss is observed with Notch(spl-1) gain-of-function mutants. Immunohistochemistry reveals that the Notch receptor is expressed in glia, whereas Delta is localized in neurons. Importantly, the expression in glia of the intracellular domain of Notch, a dominant activated form of the receptor, is sufficient to prevent learning deficits after sleep deprivation. Together, these results identify a novel neuron-glia signaling pathway dependent on Notch and regulated by bunched. These data highlight the emerging role of neuron-glia interactions in regulating both sleep and learning impairments associated with sleep loss.
| S-EPMC3741064 | biostudies-literature
Project description:Recent studies have identified the Drosophila brain circuits involved in the sleep/wake switch and have pointed to the modulation of neuronal excitability as one of the underlying mechanisms triggering sleep need. In this study we aimed to explore the link between the homeostatic regulation of neuronal excitability and sleep behavior in the circadian circuit. For this purpose, we selected Pumilio (Pum), whose main function is to repress protein translation and has been linked to modulation of neuronal excitability during chronic patterns of altered neuronal activity. Here we explore the effects of Pum on sleep homeostasis in Drosophila melanogaster, which shares most of the major features of mammalian sleep homeostasis. Our evidence indicates that Pum is necessary for sleep rebound and that its effect is more pronounced during chronic sleep deprivation (84 h) than acute deprivation (12 h). Knockdown of pum, results in a reduction of sleep rebound during acute sleep deprivation and the complete abolishment of sleep rebound during chronic sleep deprivation. Based on these findings, we propose that Pum is a critical regulator of sleep homeostasis through neural adaptations triggered during sleep deprivation.
| S-EPMC7182066 | biostudies-literature
Project description:To gain insight into the dynamic molecular processes that are altered during prolonged wakefulness and during sleep. We performed an RNA expression profiling study examining temporal changes in the brain of Drosophila in relationship to the duration of prior sleep or wakefulness. Our experimental design allowed us to determine whether genes identified as differentially regulated between sleep and wakefulness were up- or down-regulated in these states. Because stimulation of the experimental animal during the normal sleep period is used to prolong wakefulness in most experimental paradigms, the interpretation of the effects of prolonged wakefulness is confounded by the effect of the perturbation stimulus itself on the animal’s biology. We controlled for this effect in our experimental paradigm by examining gene expression changes in response to identical stimulation but during the animal’s normal wakefulness. The design of our study also allowed us to control for circadian variation in gene expression, since we compared sleeping and sleep deprived flies at the same diurnal time. Keywords: sleep deprivation, time course, stress response
2006-02-27 | GSE4174 | GEO
Project description:STUDY OBJECTIVES:Sleep is known to increase as an acute response to infection. However, the function of this behavioral response in host defense is not well understood. To address this problem, we evaluated the effect of acute sleep deprivation on post-infection sleep and immune function in Drosophila. SETTING:Laboratory. PARTICIPANTS:Drosophila melanogaster. METHODS AND RESULTS:Flies were subjected to sleep deprivation before (early DEP) or after (late DEP) bacterial infection. Relative to a non-deprived control, flies subjected to early DEP had enhanced sleep after infection as well as increased bacterial clearance and survival outcome. Flies subjected to late DEP experienced enhanced sleep following the deprivation period, and showed a modest improvement in survival outcome. Continuous DEP (early and late DEP) throughout infection also enhanced sleep later during infection and improved survival. However, improved survival in flies subjected to late or continuous DEP did not occur until after flies had experienced sleep. During infection, both early and late DEP enhanced NF?B transcriptional activity as measured by a luciferase reporter (?B-luc) in living flies. Early DEP also increased NF?B activity prior to infection. Flies that were deficient in expression of either the Relish or Dif NF?B transcription factors showed normal responses to early DEP. However, the effect of early DEP on post-infection sleep and survival was abolished in double mutants, which indicates that Relish and Dif have redundant roles in this process. CONCLUSIONS:Acute sleep deprivation elevated NF?B-dependent activity, increased post-infection sleep, and improved survival during bacterial infection.
| S-EPMC3985105 | biostudies-literature
Project description:Sleep has been proposed to be a physiological adaptation to conserve energy, but little research has examined this proposed function of sleep in humans. We quantified effects of sleep, sleep deprivation and recovery sleep on whole-body total daily energy expenditure (EE) and on EE during the habitual day and nighttime. We also determined effects of sleep stage during baseline and recovery sleep on EE. Seven healthy participants aged 22 ± 5 years (mean ± s.d.) maintained ?8 h per night sleep schedules for 1 week before the study and consumed a weight-maintenance diet for 3 days prior to and during the laboratory protocol. Following a habituation night, subjects lived in a whole-room indirect calorimeter for 3 days. The first 24 h served as baseline – 16 h wakefulness, 8 h scheduled sleep – and this was followed by 40 h sleep deprivation and 8 h scheduled recovery sleep. Findings show that, compared to baseline, 24 h EE was significantly increased by ?7% during the first 24 h of sleep deprivation and was significantly decreased by ?5% during recovery, which included hours awake 25-40 and 8 h recovery sleep. During the night time, EE was significantly increased by ?32% on the sleep deprivation night and significantly decreased by ?4% during recovery sleep compared to baseline. Small differences in EE were observed among sleep stages, but wakefulness during the sleep episode was associated with increased energy expenditure. These findings provide support for the hypothesis that sleep conserves energy and that sleep deprivation increases total daily EE in humans.
| S-EPMC3039272 | biostudies-literature
Project description:Analysis of brain of Canton-S females deprived of sleep by perturbations during their normal sleep period. Perturbation effect also assessed during their active period to control for its effect during sleep deprivation. Results suggest processes altered during prolonged wakefulness and during sleep.
2007-07-06 | E-GEOD-4174 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the SubSeries listed below.
2007-12-07 | GSE9444 | GEO