Altered hippocampal transcriptome dynamics following sleep deprivation

Widespread sleep deprivation is a continuing public health problem in the United States and worldwide affecting adolescents and adults. Acute sleep deprivation results in decrements in spatial memory and cognitive impairments. The hippocampus is vulnerable to acute sleep deprivation with changes in gene expression, cell signaling, and protein synthesis. Sleep deprivation also has long lasting effects on memory and performance that persist after recovery sleep, as seen in behavioral studies from invertebrates to humans. Although previous research has shown that acute sleep deprivation impacts gene expression, the extent to which sleep deprivation affects gene regulation remains unknown. Using an unbiased deep RNA sequencing approach, we investigated the effects of acute sleep deprivation on gene expression in the hippocampus. We identified 1,146 genes that were significantly dysregulated following sleep deprivation with 507 genes upregulated and 639 genes downregulated, including protein coding genes and long non-coding RNAs not previously identified as impacted by sleep deprivation. Notably, genes significantly upregulated after sleep deprivation were associated with RNA splicing and the nucleus. In contrast, downregulated genes were associated with cell adhesion, dendritic localization, the synapse, and postsynaptic membrane. Furthermore, we found through independent experiments analyzing a subset of genes that three hours of recovery sleep following acute sleep deprivation was sufficient to normalize mRNA abundance for most genes, although exceptions occurred for some genes that may affect RNA splicing or transcription. These results clearly demonstrate that sleep deprivation differentially regulates gene expression on multiple transcriptomic levels to impact hippocampal function.

Sleeping Disorders as a Symptom of Depression

Recently, people pay less attention to their sleep since there are a lot of stimulants to keep them awake more than sleeping. According to many reports, the results have shown that many are facing a serious condition, which is sleeping disorder. This condition is related to sleep and affects the ability to sleep well on a regular basis. It is a serious problem that if left untreated, the condition can lead to many more severe problems. There is a significant correlation between sleeping disorder and depression which is called “bidirectional relationship”. The studies show that sleeping disorders are a “symptom” of almost all types of depression such as Major Depressive Disorder, Bipolar Disorder, Seasonal Affective Disorder and so forth. On the other hand, depression itself can also be a cause of sleeping disorders. In addition, the studies show chronic sleep deprivation can cause the changes in Serotonin, which is the brain’s neurotransmitter, and will have a chance to lead to depression greater than acute sleep deprivation. As a result, people should raise awareness in sleeping and usually examine their sleep. To have less chance of depression, a person requires a healthy sleep period and effective care.

Altered hippocampal transcriptome dynamics following sleep deprivation

Widespread sleep deprivation is a continuing public health problem in the United States and worldwide affecting adolescents and adults. Acute sleep deprivation results in decrements in spatial memory and cognitive impairments. The hippocampus is vulnerable to acute sleep deprivation with changes in gene expression, cell signaling, and protein synthesis. Sleep deprivation also has long lasting effects on memory and performance that persist after recovery sleep, as seen in behavioral studies from invertebrates to humans. Although previous research has shown that acute sleep deprivation impacts gene expression, the extent to which sleep deprivation affects gene regulation remains unknown. Using an unbiased deep RNA sequencing approach, we investigated the effects of acute sleep deprivation on gene expression in the hippocampus. We identified 1,146 genes that were significantly dysregulated following sleep deprivation with 507 genes upregulated and 639 genes downregulated, including protein coding genes and long non-coding RNAs not previously identified as impacted by sleep deprivation. Notably, genes significantly upregulated after sleep deprivation were associated with RNA splicing and the nucleus. In contrast, downregulated genes were associated with cell adhesion, dendritic localization, the synapse, and postsynaptic membrane. These results clearly demonstrate that sleep deprivation differentially regulates gene expression on multiple transcriptomic levels to impact hippocampal function.

Effects of Acute Sleep Deprivation on Working Memory Capacity in Undergraduate Students

Sleep is a necessary staple in our everyday lives but with advancements in society and an increase in day to day commitments it feels as though there is not enough time in the day. One of the first things to be forsaken in the hopes of maintaining a work schedule or routine is sleep. While the lack of sleep is disproportionate in most demographics, in university students in particular, a lack of sleep is a common, consistent, and necessary plague. Students can be under the impression that the effects of sleep deprivation have mostly long-term repercussions; however, prior literature has indicated that sleep deprivation impacts not just long-term consolidation but also significantly affects memory in the short-term, specifically the working memory (Xie et al. 2019; Chee et al., 2006). In this investigation, we seek to understand the effects that acute sleep deprivation has on the working memory capacity of individuals using a 2-back spatial test. A sample of convenience of upper-class undergraduate students was chosen and the participants were asked to take a specific 2-back spatial test - twice on a day that they subjectively felt as having a regular sleep schedule and twice on a day that they subjectively felt as having sleep deprivation. The team predicted that working memory 2-back task scores will be adversely affected by sleep deprivation. While there was a statistically significant difference in the working memory scores on the full sample level, this was not reflected on the individual level. This indicates that the effects of sleep deprivation are not generalizable to a full population and that they must be reviewed on a case-by-case basis. Furthermore, since greater variation was observed in the sleep deprived scores in all individuals, it implies that sleep deprivation may indirectly affect the consistency of working memory by affecting attention span and concentration.

113 Effects of Sleep on Intrusive Symptoms and Emotion Reactivity in a Laboratory-Based Film Analogue Study

Introduction Recent literature highlights the need to focus on the impact of intrusive symptoms as a possible risk factor for the development and maintenance of PTSD. Cognitive and sleep models also contribute to the further understanding of intrusive symptoms. Further emotion work emphasizes that disgust is an emotion closely associated with the emergence of posttraumatic stress symptomology following traumatic events. Methods This study utilized a film eliciting disgust to examine the effects of acute sleep deprivation on the intensity of intrusive symptoms and emotion reactivity. Forty-nine college students were randomly assigned to sleep as usual or an acute sleep deprivation after watching a disturbing film. It was hypothesized that, relative to the control group, participants who were acutely sleep deprived would report higher frequency of intrusive symptoms and higher negative valence. Results Findings were partially consistent with hypotheses. There were no group or interaction effects on intrusive symptoms, although participants across both groups reported significant decreases in negative valence and intrusive symptoms across the study (F(1, 47) = 10.30, p < 0.01). There was a significant interaction effect between sleep group and self-reported negative valence, where individuals in the sleep deprived group reported significantly higher valence than individuals in the control group, despite significant decreases in negative valence over time (F(1, 48) = 7.869, p < 0.01). Conclusion Possible mechanisms that may contribute to the significant difference in valence may be due to higher order emotion regulation strategies that are compromised due to sleep loss. However, the significant decreases in negative valence and intrusive symptoms over time may be due to methodological factors or the type of sleep manipulation. Further work can address these challenges by using a larger sample size or examining the effects of chronic, partial sleep deprivation. Support (if any):

123 Detrimental effects of acute sleep deprivation on perceptual metacognition

Introduction Sleep deprivation (SD) impairs cognitive performance but its impact on metacognition – i.e. the ability to introspect about cognitive performance – is less clear. A few studies have assessed metacognitive accuracy after acute sleep deprivation in tasks of executive functions and found no impairments. However, whether SD has no influence on metacognition of other cognitive domains such as perception has not been investigated. In this study, we examined how metacognitive accuracy in perceptual decision tasks is affected by 32 hours of sustained wakefulness. Methods 14 participants (3 males, aged 20-32) repeated four visual psychophysical tasks (orientation discrimination, two-flicker fusion, vernier acuity and a novel face/house discrimination in noise) at regular intervals during 32 hours of sustained wakefulness and once after 8 hours recovery sleep. In each task, we concurrently measured quantitative indices of perceptual threshold, confidence rating and metacognitive accuracy (i.e. how well confidence ratings discriminate correct vs incorrect perceptual judgements). Results We observed a gradual increase of perceptual threshold in all tasks with increased time awake. Furthermore, metacognitive accuracy gradually decreased during sustained wakefulness in all tasks. Specifically, the decrease in metacognitive accuracy was driven by over-estimated confidence in trials when participants made incorrect perceptual judgements. After recovery sleep, perceptual thresholds were reset to baseline for all tasks, while metacognitive accuracy was reset to baseline for the orientation discrimination and two-flicker fusion tasks only. Conclusion We showed that sustained wakefulness up to 32 hours increasingly impairs metacognitive accuracy in perceptual decision tasks. These results are consistent across different perceptual tasks, but are in contrast to previous studies showing preserved metacognition of executive functions after SD. Overall, this suggests that the fundamental mechanisms of perceptual metacognition may be similarly affected by sleep deprivation, but that SD selectively impacts different domains of metacognition, such as perceptual metacognition and metacognition of executive functions. Support (if any) MB - Cardiff University PhD Funding CS - Wellcome Trust 209192/Z/17/Z