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Updated: Dec 11, 2025

Establishing a Device for Sleep Deprivation in Mice
Published on: September 22, 2023
DRD2 C957T genotype modulates the time-on-task effect during total sleep deprivation
Rachael A Muck1,2, Hans P A Van Dongen1,2, Michelle A Schmidt1,2
1Sleep and Performance Research Center, Washington State University, Spokane, WA, USA.
Total sleep deprivation and extended time-on-task impair cognitive performance. A specific gene variant in the dopamine D2 receptor influences how much time-on-task affects performance during sleep loss, highlighting genetic factors in sustained attention.
Area of Science:
- Neuroscience
- Genetics
- Sleep Research
Background:
- Total sleep deprivation (TSD) and prolonged time-on-task (TOT) significantly impair cognitive functions and performance.
- Individual responses to TSD and TOT vary considerably, with a portion of this variability attributable to genetic factors.
Purpose of the Study:
- To investigate the genetic underpinnings of inter-individual differences in cognitive performance during TSD and TOT.
- To determine if the dopamine receptor D2 (DRD2) C957T polymorphism influences performance decrements on a psychomotor vigilance test (PVT) under sustained sleep deprivation.
Main Methods:
- Participants underwent 38 hours of total sleep deprivation.
- Cognitive performance was assessed using the psychomotor vigilance test (PVT).
- Genotyping for the dopamine receptor D2 C957T polymorphism was performed.
Main Results:
- The dopamine receptor D2 C957T genetic polymorphism significantly predicted the magnitude of the time-on-task effect on PVT performance during 38 hours of TSD.
- Individuals with specific DRD2 genotypes exhibited differential susceptibility to performance decline with increasing time-on-task under sleep deprivation.
Conclusions:
- Dopamine availability, modulated by the DRD2 C957T polymorphism in brain regions like the striatum, plays a crucial role in the time-on-task effect during sleep loss.
- These findings suggest that dopaminergic pathways are involved in the mechanisms underlying sustained attention deficits induced by sleep deprivation.
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