The impact of sleep pressure, circadian phase and an ADA-polymorphism on working memory: a behavioral, electrophysiological, neuroimaging approach

Reichert, Carolin Franziska. The impact of sleep pressure, circadian phase and an ADA-polymorphism on working memory: a behavioral, electrophysiological, neuroimaging approach. 2015, PhD Thesis, University of Basel, Faculty of Psychology.


Official URL: http://edoc.unibas.ch/diss/DissB_11234


The need for sleep, the so-called sleep pressure, increases continuously during wakefulness and decreases during sleep again, in particular during intense deep sleep (Borbely, 1982). This sleep homeostatic process is mediated by the increase and degradation of adenosine in frontal brain structures (Porkka-Heiskanen, 2013). At the behavioural level, it is commonly mirrored in declines of performance under high sleep pressure (Cajochen, Blatter, & Wallach, 2004).
Adenosine is degraded by adenosine deaminase (ADA) (Landolt, 2008). Due to a polymorphism (rs73598374), ADA activity differs inter-individually. Lower ADA activity in G/A- compared to G/G-allele carriers (Battistuzzi, Iudicone, Santolamazza, & Petrucci, 1981)has been associated with a trait-like higher sleep pressure level, indicated by deeper sleep and worse vigilance performance (Bachmann et al., 2012).
However, the impact of sleep pressure on several sleep and waking functions depends on circadian phase (Dijk & Franken, 2005): It is potentiated during the night while counteracted during daytime by circadian wake promoting mechanisms. Also, the influence of sleep pressure on neuro-behavioral performance depends on cognitive domain (Van Dongen, Baynard, Maislin, & Dinges, 2004). Performance relying on the frontal lobes, such as executive aspects of working memory (WM), has been suggested to be particularly vulnerable to high sleep pressure (Harrison & Horne, 2000).
In a multi-methodological approach we compared thus circadian variations in sleep and in a set of waking functions according to the ADA-genotype. To capture both circadian variations and their interaction with sleep pressure, we compared two 40-h conditions, in which sleep pressure was either kept low by multiple napping (low sleep pressure) or accumulated during sleep deprivation (high sleep pressure). Nap sleep electroencephalographic (EEG) activity, vigilance, WM performance and underlying blood oxygen level-dependent (BOLD) activity was assessed in regular time intervals.
Vigilance and WM performance was worse during high as compared to low sleep pressure, particularly during the night. Specifically in executive aspects of WM, sleep pressure-dependent performance modulations were evident in G/A- but not in G/G-allele carriers (Reichert, Maire, Gabel, Viola, et al., 2014). WM performance of G/A-allele carriers benefited during napping in particular from rapid eye movement (REM) sleep duration (Reichert, Maire, Gabel, Hofstetter, et al., 2014). At times of high circadian wake promotion G/A-allele carriers showed a reduced sleep ability, indicating changes of circadian arousal promotion in response to lower ADA activity. Accordingly, we observed at a cerebral level during high circadian sleep promotion, that G/A-allele carriers showed more corti-cal compensatory mechanisms during WM performance to cope with high sleep pressure at night.
Overall, the data suggest that the impact of sleep pressure on performance, whether state- or trait-like, is modulated by circadian mechanisms. These mechanisms contribute to a differential resistance or vulnerability to sleep deprivation according to cognitive domain.
Bachmann, V., Klaus, F., Bodenmann, S., Schafer, N., Brugger, P., Huber, S., . . . Landolt, H. P. (2012). Cerebral Cortex, 22(4), 962-970. doi: bhr173 [pii]10.1093/cercor/bhr173
Borbely, A. A. (1982). A two process model of sleep regulation. Hum Neurobiol, 1(3), 195-204.
Cajochen, C., Blatter, K., & Wallach, D. (2004). Psychologica Belgica, 44(1/2), 59-80.
Dijk, D. J., & Franken, P. (2005). In R. T. Kryger MH, Dement WC (Ed.), Principles and Practice of Sleep Medicine (pp. 418-435). Philadelphia: Elsevier Saunders.
Harrison, Y., & Horne, J. A. (2000). J Exp Psychol Appl, 6(3), 236-249.
Landolt, H. P. (2008). Biochem Pharmacol, 75(11), 2070-2079. doi: 10.1016/j.bcp.2008.02.024S0006-2952(08)00104-4 [pii]
Porkka-Heiskanen, T. (2013). Curr Opin Neurobiol, 23(5), 799-805. doi: 10.1016/j.conb.2013.02.010
Reichert, C. F., Maire, M., Gabel, V., Hofstetter, M., Viola, A. U., Kolodyazhniy, V., . . . Schmidt, C. (2014). PLoS One, 9(12), e113734. doi: 10.1371/journal.pone.0113734
Reichert, C. F., Maire, M., Gabel, V., Viola, A. U., Kolodyazhniy, V., Strobel, W., . . . Schmidt, C. (2014). J Biol Rhythms, 92(2), 119-130.
Van Dongen, H. P., Baynard, M. D., Maislin, G., & Dinges, D. F. (2004). Sleep, 27(3), 423-433.
Advisors:Quervain, Dominique de
Committee Members:Cajochen, Christian
Faculties and Departments:07 Faculty of Psychology > Departement Psychologie > Abteilung Kognitive Neurowissenschaften > Cognitive Neuroscience (de Quervain)
Item Type:Thesis
Thesis no:11234
Bibsysno:Link to catalogue
Number of Pages:128 Bl.
Identification Number:
Last Modified:30 Jun 2016 10:57
Deposited On:03 Jun 2015 14:46

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