scholarly journals Altered Hypothalamic Functional Connectivity Following Total Sleep Deprivation in Young Adult Males

2021 ◽  
Vol 15 ◽  
Author(s):  
Jing Qi ◽  
Bo-Zhi Li ◽  
Ying Zhang ◽  
Bei Pan ◽  
Yu-Hong Gao ◽  
...  

Background: Sleep deprivation can markedly influence vigilant attention that is essential to complex cognitive processes. The hypothalamus plays a critical role in arousal and attention regulation. However, the functional involvement of the hypothalamus in attentional impairments after total sleep deprivation (TSD) remains unclear. The purpose of this study is to investigate the alterations in hypothalamic functional connectivity and its association with the attentional performance following TSD.Methods: Thirty healthy adult males were recruited in the study. Participants underwent two resting-state functional magnetic resonance imaging (rs-fMRI) scans, once in rested wakefulness (RW) and once after 36 h of TSD. Seed-based functional connectivity analysis was performed using rs-fMRI for the left and right hypothalamus. Vigilant attention was measured using a psychomotor vigilance test (PVT). Furthermore, Pearson correlation analysis was conducted to investigate the relationship between altered hypothalamic functional connectivity and PVT performance after TSD.Results: After TSD, enhanced functional connectivity was observed between the left hypothalamus and bilateral thalamus, bilateral anterior cingulate cortex, right amygdala, and right insula, while reduced functional connectivity was observed between the left hypothalamus and bilateral middle frontal gyrus (AlphaSim corrected, P < 0.01). However, significant correlation between altered hypothalamic functional connectivity and PVT performance was not observed after Bonferroni correction (P > 0.05).Conclusion: Our results suggest that TSD can lead to disrupted hypothalamic circuits, which may provide new insight into neural mechanisms of attention impairments following sleep deprivation.

Life ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1110
Author(s):  
Mégane Erblang ◽  
Catherine Drogou ◽  
Danielle Gomez-Merino ◽  
Arnaud Rabat ◽  
Mathias Guillard ◽  
...  

Several genetic polymorphisms differentiate between healthy individuals who are more cognitively vulnerable or resistant during total sleep deprivation (TSD). Common metrics of cognitive functioning for classifying vulnerable and resilient individuals include the Psychomotor Vigilance Test (PVT), Go/noGo executive inhibition task, and subjective daytime sleepiness. We evaluated the influence of 14 single-nucleotide polymorphisms (SNPs) on cognitive responses during total sleep deprivation (continuous wakefulness for 38 h) in 47 healthy subjects (age 37.0 ± 1.1 years). SNPs selected after a literature review included SNPs of the adenosine-A2A receptor gene (including the most studied rs5751876), pro-inflammatory cytokines (TNF-α, IL1-β, IL-6), catechol-O-methyl-transferase (COMT), and PER3. Subjects performed a psychomotor vigilance test (PVT) and a Go/noGo-inhibition task, and completed the Karolinska Sleepiness Scale (KSS) every 6 h during TSD. For PVT lapses (reaction time >500 ms), an interaction between SNP and SDT (p < 0.05) was observed for ADORA2A (rs5751862 and rs2236624) and TNF-α (rs1800629). During TSD, carriers of the A allele for ADORA2A (rs5751862) and TNF-α were significantly more impaired for cognitive responses than their respective ancestral G/G genotypes. Carriers of the ancestral G/G genotype of ADORA2A rs5751862 were found to be very similar to the most resilient subjects for PVT lapses and Go/noGo commission errors. Carriers of the ancestral G/G genotype of COMT were close to the most vulnerable subjects. ADORA2A (rs5751862) was significantly associated with COMT (rs4680) (p = 0.001). In conclusion, we show that genetic polymorphisms in ADORA2A (rs5751862), TNF-α (rs1800629), and COMT (rs4680) are involved in creating profiles of high vulnerability or high resilience to sleep deprivation. (NCT03859882).


2021 ◽  
Vol 12 ◽  
Author(s):  
Ying Zhang ◽  
Cimin Dai ◽  
Yongcong Shao ◽  
Jiaxi Peng ◽  
Yan Yang ◽  
...  

Sleep deprivation (SD) induces a negative emotional experience due to a prolonged time spent awake. However, few studies have focused on the mechanism underlying communication within brain networks or alterations during this emotional deterioration. We propose that negative reward judgment is important in poor emotional processing after SD, which will be reflected in functional connectivity in the reward network. We sought to analyze alterations in functional connectivity within the reward network and cerebral cortex. Furthermore, we analyzed changes in functional connectivity correlation with negative emotional experience after SD. Twenty-six healthy volunteers participated in this study. Two resting-state fMRI scans were obtained from the participants, once during resting wakefulness, and once after 36 h of total SD. The bilateral nucleus accumbens (NAc) was selected as a seed region for region of interest (ROI)-to-ROI functional connectivity analysis. Correlation analyses between functional connectivity alterations within the reward network and negative emotional experience were also performed. We found that SD decreased functional connectivity between the left NAc and anterior cingulate cortex (ACC) compared with resting wakefulness. There was a decreased functional connectivity with the ACC and right inferior frontal gyrus (IFG) after SD in the right NAc. Furthermore, decreased functional connectivity between the right NAc and right IFG, and NAc and ACC was negatively correlated with emotional experience scores. Sleep deprivation decreased functional connectivity within the reward network. This may be associated with the enhanced negative emotional experience that was found after total sleep deprivation.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Eric Chern-Pin Chua ◽  
Jason P. Sullivan ◽  
Jeanne F. Duffy ◽  
Elizabeth B. Klerman ◽  
Steven W. Lockley ◽  
...  

Genes ◽  
2021 ◽  
Vol 12 (4) ◽  
pp. 555
Author(s):  
Mégane Erblang ◽  
Fabien Sauvet ◽  
Catherine Drogou ◽  
Michaël Quiquempoix ◽  
Pascal Van Beers ◽  
...  

This study investigated whether four single nucleotide polymorphisms (SNPs) moderated caffeine effects on vigilance and performance in a double-blind and crossover total sleep deprivation (TSD) protocol in 37 subjects. In caffeine (2 × 2.5 mg/kg/24 h) or placebo-controlled condition, subjects performed a psychomotor vigilance test (PVT) and reported sleepiness every six hours (Karolinska sleepiness scale (KSS)) during TSD. EEG was also analyzed during the 09:15 PVT. Carriers of the TNF-α SNP A allele appear to be more sensitive than homozygote G/G genotype to an attenuating effect of caffeine on PVT lapses during sleep deprivation only because they seem more degraded, but they do not perform better as a result. The A allele carriers of COMT were also more degraded and sensitive to caffeine than G/G genotype after 20 h of sleep deprivation, but not after 26 and 32 h. Regarding PVT reaction time, ADORA2A influences the TSD effect but not caffeine, and PER3 modulates only the caffeine effect. Higher EEG theta activity related to sleep deprivation was observed in mutated TNF-α, PER3, and COMT carriers, in the placebo condition particularly. In conclusion, there are genetic influences on neurobehavioral impairments related to TSD that appear to be attenuated by caffeine administration. (NCT03859882).


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.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A116-A116
Author(s):  
R A Muck ◽  
L Skeiky ◽  
M A Schmidt ◽  
B C Satterfield ◽  
J P Wisor ◽  
...  

Abstract Introduction There are substantial, phenotypical individual differences in the adverse impact of total sleep deprivation (TSD) on vigilant attention performance. Dopaminergic genotypes have been found to contribute to these phenotypical differences. Here we investigated the association between a single nucleotide polymorphism (SNP) of the dopamine receptor D2 (DRD2) gene, C957T (rs6277), on vigilant attention performance measured with the psychomotor vigilance test (PVT) in a laboratory TSD study. Methods N=46 healthy adults (ages 26.0±5.3y; 25 females) completed a 4-day in-laboratory study with a baseline day (10h time in bed: 22:00-08:00), a 38h TSD period, and a recovery day (10h time in bed: 22:00-08:00). DNA isolated from whole blood was assayed for DRD2 C957T genotype using real-time polymerase chain reaction. PVT performance was measured during TSD at 2-4h intervals, and analyzed for genotype using mixed-effects analysis of covariance of lapses of attention (RTs&gt;500ms). Results The genotype distribution in this sample - 28.3% C/C, 50.0% C/T, 21.7% T/T - was found to be in Hardy-Weinberg Equilibrium (X21=0.0008, p=0.98). As expected, there was a significant effect of time awake on PVT performance (F14,602=26.67, p&lt;0.001). There was a significant main effect of DRD2 genotype (F2,602=3.24, p=0.040) and a significant interaction of time awake by DRD2 genotype (F28,602=1.96, p=0.003). Subjects homozygous for the T allele showed greater impairment during extended wakefulness than carriers of the C allele. Genotype explained 7.6% of the variance in the PVT data observed during the 38h TSD period. Conclusion Subjects homozygous for the T allele of DRD2 C957T were considerably more vulnerable to TSD-induced PVT performance impairment than carriers of the C allele. A recent study showed that DRD2 C957T influences PVT performance in interaction with a SNP of the DAT1 gene. Here, DRD2 genotype was by itself also associated with PVT performance impairment during TSD. Support CDMRP awards W81XWH-16-1-0319 and W81XWH-18-1-0100.


SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A112-A112
Author(s):  
A K Skwara ◽  
L Skeiky ◽  
H Van Dongen ◽  
D A Hansen

Abstract Introduction While measuring the neurobehavioral consequences of sleepiness is arguably best done with performance tasks providing objective assessments of impairment, this often proves challenging in real-world operational settings. Self-report instruments measuring subjective sleepiness provide a practical alternative, but field studies generally fail to show high correlation between objective and subjective assessments of impairment. The Sleepiness Symptoms Questionnaire (SSQ) is a self-report instrument developed to address this issue by asking about observable symptoms of sleepiness and (motor vehicle driving) performance impairment. In a laboratory sleep deprivation study, we compared SSQ sleepiness ratings to performance impairment on a 10min psychomotor vigilance test (PVT). Methods N=12 healthy normal sleepers (ages 21-39y, 6 females) participated in a 4-day in-laboratory study. After a baseline day (9h time in bed; 22:00-07:00), subjects underwent 38h total sleep deprivation (TSD) followed by a recovery day (9h time in bed; 22:00-07:00). As part of neurobehavioral testing throughout the experiment, subjects completed the SSQ and PVT back to back at 6.5h, 14.5h, 22.5h, and 30.5h TSD, and 6.5h after recovery sleep. Data from one subject were incomplete and discarded prior to analysis. Results As TSD progressed, the SSQ sleepiness ratings and the number of lapses (RTs&gt;500ms) on the PVT were elevated, with sleepiness and performance impairment peaking at 22.5h TSD. Both measures returned to baseline levels after recovery sleep. Mixed-effects analysis of covariance showed moderate correlation between SSQ ratings and PVT lapses (r=0.44, F1,43=24.1, p&lt;0.001). Conclusion Self-reported sleepiness on the SSQ reflected the expected homeostatic and circadian changes in sleep pressure during TSD and following recovery sleep, as did PVT performance impairment. The moderate correlation between subjective ratings on the SSQ, with its emphasis on observable sleepiness symptoms, and objective impairment on the PVT suggests that the SSQ may be a reasonably reliable instrument for measuring sleepiness under conditions of acute sleep deprivation. Support Jazz Pharmaceuticals


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