040 Sleep Deprivation Disrupts Binding of Information with Its Context

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A17-A18
Author(s):  
Courtney Kurinec ◽  
Paul Whitney ◽  
John Hinson ◽  
Devon Hansen ◽  
Hans Van Dongen

Abstract Introduction Effective memory often requires recall of both specific information and the context in which the information was encountered. Total sleep deprivation (TSD) is known to impair memory for information items (e.g., words on a studied list), but the impact of TSD on binding, or associative linking, between items and context is not clear. Methods N=68 healthy adults (ages 22–40; 35 females) completed a 4-day (3-night) in-laboratory study. After a baseline night with 10h nighttime sleep opportunity, participants were randomly assigned to either 38h TSD (n=38) or a well-rested control (WRC) condition with 10h nighttime sleep opportunity (n=30). Both study arms concluded with a 10h nighttime recovery sleep opportunity. Participants completed a standardized recognition memory task at 14:50 on day 2 (baseline, session 1) and again 24h later (session 2). The memory task consisted of a study phase in which words with negative, positive, and neutral affective valence were spoken by a female or male speaker (50% each); followed immediately by a test phase, in which subjects made recognition judgments for the items (words) and their source (speaker). Results Mixed-effects ANOVA revealed significant interactions of session by condition for both word and speaker recognition (p<0.001). When sleep-deprived, TSD participants recognized fewer words and, for words that were correctly recognized, they were worse at recognizing the speaker, compared to baseline and to the WRC group. Negatively valenced words were associated with poorer word recognition (p<0.001), and in session 1 poorer source recognition (p = 0.032), but these valence effects did not interact with sleep deprivation. Conclusion TSD impaired memory for items, but more importantly, also impaired memory for the context in which items were presented, even if the items were themselves correctly recognized, and regardless of their affective valence. These results indicate that TSD may disrupt binding of information to its context, which could explain TSD deficits in decision-making tasks that require novel associative linking. Furthermore, our findings are important in real-world situations such as eyewitness accounts and perseveration of the influence of misinformation. Support (if any) NIH grant R21 CA167691 and CDMRP award W81XWH-20-1-0442

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A48-A48
Author(s):  
A N Hudson ◽  
P Whitney ◽  
J M Hinson ◽  
D A Hansen ◽  
H Van Dongen ◽  
...  

Abstract Introduction Stimuli with an emotional valence tend to produce better recognition from memory than neutral stimuli. Sleep loss is believed to increase reactivity to negative stimuli, as compared to positive stimuli, which may comparatively enhance subsequent recognition from memory for negative stimuli. We investigated the impact of total sleep deprivation (TSD) on recognition accuracy for words with different emotional valence using the Affective Item Source Memory Task (AISM). Methods N=14 adults (ages 21–39; 7 females) completed a 4-day in-laboratory study with 9h baseline sleep (22:00-07:00), 39h acute TSD, and 9h recovery sleep. The AISM was administered at 16:30 during baseline and after 34h TSD. During a 5min study phase, participants heard a list, twice, of 20 positive, 20 negative, and 20 neutral words spoken with a male or female voice. During an immediately subsequent 8min recognition phase, participants heard 120 words (50% new) and judged whether each word had been presented in the study list (item memory). For words judged to have been presented previously, participants indicated whether those were presented by a female or male speaker (source memory). Results Mixed-effects ANOVA showed effects of session (p<0.001) and valence (p<0.001) on item memory. At baseline, accuracy was greatest for neutral and positive words compared to negative words. During TSD, accuracy declined for all three valences, and no interaction of session by valence was detected. No effects of TSD or valence on source memory were observed. Conclusion Sleep deprivation reduced item memory for words of all valence types. However, there was no comparatively greater impact on item or source memory for negative words nor any differential effect of TSD for different valences. Whether our results would hold with longer time intervals between task phases or an intervening sleep period remains to be determined. Support Jazz Pharmaceuticals


SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A18-A18
Author(s):  
Sara Alger ◽  
John Hughes ◽  
Thomas Balkin ◽  
Tracy Jill Doty

Abstract Introduction Threat-related information is preferentially processed, facilitating quick and efficient responses. However, the impact of extended sleep deprivation on perception of and response to threatening information is not well known. Sleep loss may increase amygdalar activity and negative mood, potentially facilitating threat processing. However, it also reduces cognitive function, possibly impairing ability to respond. The present study assessed the extent to which extended sleep deprivation modulates threat processing using a threat expectation paradigm. Methods Twenty-one participants underwent one baseline night of sleep followed by 62hrs total sleep deprivation (TSD) and one recovery night of sleep (12hrs). Threat expectation task performance was assessed at baseline, at multiple time points during TSD, and following recovery sleep. To control for circadian influence, performance at three 1100 sessions (baseline, 52hrs into TSD, and recovery) were compared. The threat expectation task involved determining whether a presented face was fearful (i.e., signaled threat) or neutral. Faces were presented at three expectation levels: 80%, 50%, and 20% chance of viewing a fearful face. Results Overall, responses were faster (F=9.77, p=0.001) and more accurate (F=11.48, p=0.001) when the type of face (fearful or neutral) was expected. Accuracy significantly decreased over TSD (t=7.71, p<0.001) and recovered following subsequent sleep. Fear bias was calculated for accuracy (accuracy for fearful face minus neutral face). Under conditions of high expectation (80%) of viewing a fearful face, fear bias increased across TSD (t=-1.95, p=0.07). Although accuracy to both fearful and neutral faces significantly declined across TSD (both p<0.001), decline for neutral faces was greater, thus increasing fear bias. Importantly, the increased bias toward fear was still evident compared to baseline following a 12-hour recovery sleep opportunity, (t=-1.93, p=0.07). Conclusion Extended sleep deprivation, common in operational environments where there is also high expectation of encountering threat, impairs cognitive control and is thought to enhance amygdala activity. These data show that, consequently, cognitive resources become biased toward biologically adaptive behaviors (i.e., threat processing) at the expense of attending and responding more broadly to all stimuli. This behavior is not reversed with a single extended sleep opportunity. Support (if any) Department of Defense Military Operational Medicine Research Program (MOMRP)


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A117-A117
Author(s):  
T J Cunningham ◽  
R M Bottary ◽  
E A Kensinger ◽  
R Stickgold

Abstract Introduction The ability to perceive emotions is a socially-relevant skill critical for healthy interpersonal functioning, while deficits in this ability are associated with psychopathology. Total sleep deprivation (TSD) has been shown to have deleterious effects on emotion perception, yet the extent to which these impairments persist across the day with continued wakefulness, or if brief periods of recovery sleep can restore emotion perception abilities, remains unexplored. Methods Participants viewed slideshows of faces ranging in emotional expression and were asked to categorize (Happy, Sad, Angry, Neutral) and rate the emotional intensity (1-9) of each face at baseline (2100; Session 1), at 0900 (Session 2) following a night of sleep or TSD, and at 1400 (Session 3) following either continued wakefulness (wake group) or a 90-minute nap opportunity (nap group). Results Emotion categorization ability marginally improved from Session 1 to Session 2 following overnight sleep, however, no changes in emotion intensity ratings or vigilance were observed. TSD led to an increase in error rates during vigilance testing [t(46)=2.9, p=0.005] and impairment in emotion categorization ability [t(46)=5.5, p<0.001] from Session 1 to Session 2, although by Session 3 performance levels on both measures returned to baseline for all TSD participants. TSD also led to a decrease in emotional intensity ratings from Session 1 to Session 2, particularly for the highest tertile of emotional faces [6-9; t(46)=6.1, p<0.001]. These ratings remained suppressed at Session 3 in both the wake [t(25)=7.8, p<0.001] and nap [t(18)=3.1, p=0.006] groups. Conclusion These results indicate that time of day effects, with or without any additional benefit of a nap, can restore the impairments in vigilance and emotional categorization caused by TSD. The ability to discriminate levels of emotional intensity, however, is not restored by time of day or napping, suggesting that this ability is more sensitive to the impact of TSD. Support  


eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Robbert Havekes ◽  
Alan J Park ◽  
Jennifer C Tudor ◽  
Vincent G Luczak ◽  
Rolf T Hansen ◽  
...  

Brief periods of sleep loss have long-lasting consequences such as impaired memory consolidation. Structural changes in synaptic connectivity have been proposed as a substrate of memory storage. Here, we examine the impact of brief periods of sleep deprivation on dendritic structure. In mice, we find that five hours of sleep deprivation decreases dendritic spine numbers selectively in hippocampal area CA1 and increased activity of the filamentous actin severing protein cofilin. Recovery sleep normalizes these structural alterations. Suppression of cofilin function prevents spine loss, deficits in hippocampal synaptic plasticity, and impairments in long-term memory caused by sleep deprivation. The elevated cofilin activity is caused by cAMP-degrading phosphodiesterase-4A5 (PDE4A5), which hampers cAMP-PKA-LIMK signaling. Attenuating PDE4A5 function prevents changes in cAMP-PKA-LIMK-cofilin signaling and cognitive deficits associated with sleep deprivation. Our work demonstrates the necessity of an intact cAMP-PDE4-PKA-LIMK-cofilin activation-signaling pathway for sleep deprivation-induced memory disruption and reduction in hippocampal spine density.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A418-A419
Author(s):  
O Galli ◽  
N Goel ◽  
M Basner ◽  
J Detre ◽  
M Thase ◽  
...  

Abstract Introduction Negativity bias in depression has been repeatedly demonstrated in the judgment and decision-making literature. Research investigating the impact of sleep deprivation on self-evaluation of performance in healthy or depressed populations is limited. We examined 1) whether individuals with Major Depressive Disorder (MDD) exhibit a negativity bias in subjective ratings of performance on the Psychomotor Vigilance Task (PVT) as compared with healthy adults, and 2) the impact of total sleep deprivation (TSD) on these ratings. Methods N=33 individuals with MDD and n=9 healthy adults completed a 5-day study protocol including two baseline nights (B1-B2, 9h TIB), 36 hours of TSD, and one night of recovery sleep opportunity (Rec). The PVT was administered every 2-4 hours. A brief questionnaire was administered immediately prior to (PRE) and following (POST) the PVT, asking participants to estimate their average reaction time (RT) using a 9-point Likert-type scale. Mixed-effects models examined the impact of group (MDD, Control), protocol day (B1, B2, SD, Rec), and their interaction on objective PVT performance (mean RT) and subjective performance estimates (PRE and POST ratings). Results Mean RT was significantly slower during TSD (p<0.001) for all participants. Individuals with MDD and healthy adults did not differ in objective PVT performance (p=0.25) across days. There was no significant interaction between group and protocol day (p=0.96). Both groups predicted slower RTs during TSD as compared with baseline or recovery days (PRE-PVT, p=0.006). Individuals with MDD anticipated slower RTs as compared with healthy adults (p=0.001). On POST-PVT estimates, all participants reported subjective poorer performance during TSD (p<0.008). Individuals with MDD reported slower RTs as compared with healthy adults (p=0.002). Interaction effects between group and protocol day on PRE- and POST- performance ratings were not significant. Conclusion This project is the first to investigate subjective estimates of PVT performance in healthy and depressed individuals. Individuals with MDD subjectively reported slower response times as compared with control participants, despite similar objective performance. Depressive symptoms may be a potential confounder of subjective, but not objective, PVT performance. Support 5R01MH107571


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A40-A41
Author(s):  
A V Guttesen ◽  
G Appleby ◽  
E Madden ◽  
M Gaskell ◽  
S A Cairney

Abstract Introduction Contemporary models of sleep-associated consolidation posit that overnight memory processing paves the way for next-day learning in hippocampus. However, the extent to which new hippocampal learning is dependent on overnight consolidation has yet to be investigated. In this study, we compared the impacts of sleep and sleep deprivation on the consolidation and encoding of hippocampus-dependent memories and, importantly, examined whether individual differences in consolidation were associated with individual differences in encoding. Methods Thirty healthy adults (17 females, mean age 20.1±1.65) were trained on a spatial memory task in the evening before a night of sleep or total sleep deprivation (repeated measures). Participants completed a spatial memory test the following morning, and then encoded a novel set of word-image pairs. Two days later (after recovery sleep), memory for the word-image pairs was tested. We predicted that participants’ spatial memory recall would predict performance on the word-image test, suggesting that overnight consolidation lays the groundwork for new encoding in hippocampus. Results Sleep (vs. sleep deprivation) improved spatial memory accuracy the following morning (t(29)=3.93, p<.001, d=0.72) and word-image recall two days later (t(29)=12.19, p<.001, d=2.23), suggesting that sleep facilitated the consolidation and encoding of hippocampus-dependent memories, respectively. However, the benefit of sleep for spatial memory recall was not significantly correlated with the benefit of sleep for word-image encoding (r(28)= 0.01, p=0.971), suggesting that hippocampal encoding was not contingent on foregoing overnight consolidation processes. Conclusion In support of previous findings, overnight sleep improved consolidation and next-day encoding, as compared to an equivalent period of sleep deprivation. However, the present results did not reveal any relationship between an individual’s sleep-associated consolidation and their next-day learning. Support Department of Psychology, University of York scholarship to A.áV.G. Medical Research Council Career Development Award (MR/P020208/1) to S.A.C.


2020 ◽  
Author(s):  
Zi-Yi Peng ◽  
Yi Wang ◽  
Ci-Min Dai ◽  
Le-Tong Wang ◽  
Song-Yue Xie ◽  
...  

Abstract Background: Considering the well-known detrimental effects of sleep deprivation (SD) on cognitive function and quality of life, sleep disturbances represent a major physical and mental health issue. Because working memory plays an important role in many complex cognitive processes, it is necessary to identify strategies that can effectively counteract the negative effects of SD on working memory. Methods: In the present study, we utilized event-related potentials (ERPs) to investigate the restorative effect of 8 h of recovery sleep (RS) on working memory impairments induced by 36 h of total sleep deprivation (TSD). We analyzed data from 16 healthy male participants. All participants completed a 2-back working memory task before and after 36 h of TSD and after 8 h of RS. Electroencephalography (EEG) data were recorded during the task. Results: N2 and P3 components related to working memory exhibited low-amplitude slow-wave characteristics following 36 h of TSD. Significant decreases in the latency of the N2 component were observed after 8 h of RS. RS also induced significant increases in the amplitude of the P3 component, along with significant decreases in P3 latency. Conclusions: Eight hours of RS also attenuated decreases in working memory performance caused by 36 h of TSD. However, the effects of RS appear to be limited.


2019 ◽  
Author(s):  
Jennifer R Sadler ◽  
Grace Elisabeth Shearrer ◽  
Nichollette Acosta ◽  
Kyle Stanley Burger

BACKGROUND: Dietary restraint represents an individual’s intent to limit their food intake and has been associated with impaired passive food reinforcement learning. However, the impact of dietary restraint on an active, response dependent learning is poorly understood. In this study, we tested the relationship between dietary restraint and food reinforcement learning using an active, instrumental conditioning task. METHODS: A sample of ninety adults completed a response-dependent instrumental conditioning task with reward and punishment using sweet and bitter tastes. Brain response via functional MRI was measured during the task. Participants also completed anthropometric measures, reward/motivation related questionnaires, and a working memory task. Dietary restraint was assessed via the Dutch Restrained Eating Scale. RESULTS: Two groups were selected from the sample: high restraint (n=29, score >2.5) and low restraint (n=30; score <1.85). High restraint was associated with significantly higher BMI (p=0.003) and lower N-back accuracy (p=0.045). The high restraint group also was marginally better at the instrumental conditioning task (p=0.066, r=0.37). High restraint was also associated with significantly greater brain response in the intracalcarine cortex (MNI: 15, -69, 12; k=35, pfwe< 0.05) to bitter taste, compared to neutral taste.CONCLUSIONS: High restraint was associated with improved performance on an instrumental task testing how individuals learn from reward and punishment. This may be mediated by greater brain response in the primary visual cortex, which has been associated with mental representation. Results suggest that dietary restraint does not impair response-dependent reinforcement learning.


SLEEP ◽  
2020 ◽  
Author(s):  
Erika M Yamazaki ◽  
Caroline A Antler ◽  
Charlotte R Lasek ◽  
Namni Goel

Abstract Study Objectives The amount of recovery sleep needed to fully restore well-established neurobehavioral deficits from sleep loss remains unknown, as does whether the recovery pattern differs across measures after total sleep deprivation (TSD) and chronic sleep restriction (SR). Methods In total, 83 adults received two baseline nights (10–12-hour time in bed [TIB]) followed by five 4-hour TIB SR nights or 36-hour TSD and four recovery nights (R1–R4; 12-hour TIB). Neurobehavioral tests were completed every 2 hours during wakefulness and a Maintenance of Wakefulness Test measured physiological sleepiness. Polysomnography was collected on B2, R1, and R4 nights. Results TSD and SR produced significant deficits in cognitive performance, increases in self-reported sleepiness and fatigue, decreases in vigor, and increases in physiological sleepiness. Neurobehavioral recovery from SR occurred after R1 and was maintained for all measures except Psychomotor Vigilance Test (PVT) lapses and response speed, which failed to completely recover. Neurobehavioral recovery from TSD occurred after R1 and was maintained for all cognitive and self-reported measures, except for vigor. After TSD and SR, R1 recovery sleep was longer and of higher efficiency and better quality than R4 recovery sleep. Conclusions PVT impairments from SR failed to reverse completely; by contrast, vigor did not recover after TSD; all other deficits were reversed after sleep loss. These results suggest that TSD and SR induce sustained, differential biological, physiological, and/or neural changes, which remarkably are not reversed with chronic, long-duration recovery sleep. Our findings have critical implications for the population at large and for military and health professionals.


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