|Reference : Influence of sleep homeostasis and circadian rhythm on executive discriminative abili...|
|Scientific congresses and symposiums : Poster|
|Life sciences : Genetics & genetic processes|
Human health sciences : Neurology
|Influence of sleep homeostasis and circadian rhythm on executive discriminative ability during a constant routine|
|Jaspar, Mathieu [Université de Liège - ULg > Département de Psychologie : cognition et comportement; Centre de recherches du cyclotron; WELBIO, Belgium > Neuropsychologie > >]|
|Meyer, Christelle [Université de Liège - ULg > > Centre de recherches du cyclotron; WELBIO, Belgium > >]|
|Muto, Vincenzo [Université de Liège - ULg > Département de Psychologie > Centre de recherches du cyclotron; WELBIO, Belgium > >]|
|Shaffii, Anahita [Université de Liège - ULg > > Centre de recherches du cyclotron >]|
|Chellappa, Sarah Laxhmi [Université de Liège - ULg > > Centre de recherches du cyclotron >]|
|Vandewalle, Gilles [Université de Liège - ULg > > Centre de recherches du cyclotron >]|
|Collette, Fabienne [Université de Liège - ULg > Département de Psychologie : cognition et comportement > Neuropsychologie >]|
|Archer, Simon [Surrey Sleep Research Centre, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK > > > >]|
|Dijk, Derk-Jan [Surrey Sleep Research Centre, Faculty of Health and Medical Sciences, University of Surrey, Guildford, UK > > > >]|
|MAQUET, Pierre [Centre Hospitalier Universitaire de Liège - CHU > > Neurologie Sart Tilman >]|
|21st Congress of the European Sleep Research Society|
|4 - 8 September 2012|
|[en] Sleep ; gene PERIOD3 (PER3) ; circadian rhythms|
|[en] Introduction & Objectives
The human brain upholds cognitive performance throughout a waking day due to putative circadian (C) arousal signal (1) which counteracts the increase in homeostatic (H) sleep pressure associated to the deterioration in brain efficiency. When wakefulness is extended into the circadian night, maintenance of cognitive performance is jeopardized (Fig.1). Some individuals are very vulnerable to the negative effects of sleep loss and circadian misalignment, whereas others are resilient (3). These individuals differences can be readily explained within the conceptual framework of the circadian and homeostatic regulation of performance (4,5) but also by individual genetic differences and notably the PERIOD3 gene polymorphism (6).
In this experiment, we investigated the consequences of sleep deprivation on cognitive performance during a working memory task (3-back). Following the signal detection theory, the ability to discriminate target from non-target stimuli is estimated by d prime (d') and criterion (cr). Here we assessed whether d' and cr were modulated by the raising sleep need and the oscillatory circadian signal. We also tested whether the individual vulnerability to sleep loss predicted by the PERIOD3 gene polymorphism influences this cognitive modulation, which is also driven by the sleep/wake regulation.
Materials and Methods
Population: Thirty-five right-handed healthy young volunteers aged from 19 to 26 (17 females) were recruited on the basis of their PER3 polymorphism. From a sample of about 400 screened volunteers, twelve 5/5 and twenty-three 4/4 homozygotes (matched for age, gender, chronotype, IQ, and level of education at the group level) participated in this study.
Study protocol: Participants wore actigraphs for three weeks before the laboratory study. The first two weeks allowed us to determine their habitual sleep/wake schedule. During the third one, a strict sleep schedule adjusted on two possible timetables (00:00-08:00 or 01:00-09:00) was imposed in order to stagger fMRI sessions. Compliance to this schedule was again checked by wrist actigraphy and sleep diaries. The laboratory study began in the evening of day 1 and ran over 5 nights (Fig. 2). During the first 2 nights (habituation and baseline), the volunteers slept according to habitual sleep/wake schedule. Participants remained awake from the morning of day 3 for 42 hours. During this period, they remained in a semi-recumbent position, under dim light conditions (5 lux, eye level), with no information on clock time, in a constant routine protocol (CR). Saliva samples was hourly collected for melatonin analysis. Every 2 hours, volunteers received calibrated isocaloric snacks, behavioral data were collected and waking EEG recorded.
During CR, behavioral measures were used to assess subjective (Karolinska Sleepiness Scale, KSS) and objective alertness (psychomotor vigilance task [PVT]). Executive functioning efficiency was assessed using the 3-back (Fig. 3) and SART tasks. During fMRI, participants performed alternating blocks of 0- and 3-back task.
D’ and cr (Fig. 4) were analyzed with mixed-model analysis of variance (PROC Mixed), with main factors “session” and “genotype” (PER3 4/4 & PER3 5/5). All p-values derived from r-ANOVAs were based on Huynh-Feldt's (H-F) corrected degrees of freedom (p<0.05). Exploratory analysis assessed theoretical coefficients for the homeostatic sleep pressure (derived from a quasi-linear function) and the circadian oscillation (as a 24-hour period sine wave) were utilized in a multiple regression model to predict d’ and cr performance during the CR. Before these analyses, d’ and cr have been normalized using a z-score transformation.
Analyses on d’
1. MIXED MODEL :
Significant effect of sessions (F(12,385) = 17.16, p < 0.0001), but no group effect (F(1,133) = 0.00, p = 0.99) or interaction (F(12,385) = 1.51, p = 0.11).
Significant regression (R² = 0.24, F(2,440) = 69.94, p <0.0001). The two predictors are significant (homeostat: p < 0.0001 ; circadian: p < 0.0001).
Analyses on cr
1. MIXED MODEL :
Significant effect of sessions (F(12,385) = 4.12, p < 0.0001), but no group effect (F(1,133) = 0.00, p = 0.99) or interaction (F(12,385) = 0.75, p = 0.71).
Significant regression (R² = 0.04, F(2,440) = 9.35 , p = 0.0001). Only one predictor was significant (homeostat: p < 0.0001 ; circadian: p = 0.96).
These preliminary results show that both sleep homeostatic pressure and circadian factors influence executive discriminative ability during sleep loss, as assessed by signal detection theory (d’).
Decision criterion (cr) appears modulated only by homeostatic sleep pressure. The difference between these two parameters could be explained by the theoretical modeling of the circadian oscillation and future analyses will incorporate individual experimentally-derived homeostatic and circadian parameters.
Neither discrimination ability (d’) or criterion (cr) seem sensitive measures of individual cognitive vulnerability to sleep loss predicted by PER3 polymorphism.
(1) Aston-Jones. Sleep Med. 2005, 6(Suppl 1), S3-7. (2) Dijk & Archer. Sleep Med. Rev. 2010, 14, 151-160.(3) Van Dongen & al. Sleep. 2004, 27, 423-433. (4) Mongrain & al. J. Sleep Res. 2006, 15, 162-166. (5) Van Dongen et al. Sleep. 2007, 30, 1129-1143. (6) Groeger & al. Sleep. 2008, 31, 1159-1167. (7) Vandewalle & al. J. Neuro. 2009, 29, 7948-7956.
ACKNOWLEDGEMENTS & SPONSORS
Cyclotron Research Centre (CRC) ; Belgian National Funds of Scientific Research (FNRS) ; Actions de Recherches Concertées (ARC, ULg) – Fondation Médicale Reine Elisabeth (FMRE) ; Walloon Excellence in Lifesciences and Biotechnology (WELBIO) ; Wellcome Trust ; Biotechnology and Biological Sciences Research Council (BBSRC)
|Cyclotron Research Centre, University of Liège, Belgium|
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