Increased Metabotropic Glutamate Receptor Subtype 5 Availability in Human Brain After One Night Without Sleep

Hefti, Katharina; Holst, Sebastian C.; Sóvágó, Judit; Bachmann, Valérie; Buck, Alfred; Ametamey, Simon M.; Scheidegger, Milan; Berthold, Thomas; Gomez‐Mancilla, Baltazar; Seifritz, Erich; Landolt, Hans‐Peter

doi:10.1016/j.biopsych.2012.07.030

Cited by 86 publications

(68 citation statements)

References 55 publications

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“…Concerted activation of both mGlu5 and A 2A receptors in these receptor heteromers may, therefore, efficiently reduce arousal and promote sleep. In accordance with this hypothesis, the functional availability of mGlu5 receptors in a striatal region including the NAc is enhanced compared to baseline after the experimental deprivation of one night of sleep in humans [105]. Intriguingly, the same procedure was found to reduce dopamine D 2/3 receptor availability in the ventral striatum by almost the identical magnitude (~5 %) [100].…”

Section: Adenosine Receptor Heteromers and Receptor-receptor Interactmentioning

confidence: 55%

Sleep Homeostasis, Metabolism, and Adenosine

Holst

Landolt

2015

Curr Sleep Medicine Rep

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Sleep is an integral and constitutive part of life, invariably observed in animals with even a simple nervous system. Importantly, sleep is an active and highly regulated state. Sleep propensity or sleep need and its best established biological marker, electroencephalographic (EEG) slow-wave (or delta) activity, is tightly associated to prior wakefulness and sleep and is homeostatically regulated. Sleep need may be considered an essential aspect of life, just like feeding, drinking, and procreation. Sleep, therefore, likely developed in a primordial state of evolution and should either aid or, at least, not interfere with other essential biological aspects of life such as metabolisms and reproduction. Consistent with this view, brain circuitries regulating sleep need, metabolism, and reward appear to involve the basal ganglia and are tightly linked. They may sense changes in the organism's major cellular energy store, adenosine-tri-phosphate (ATP), and its derivative adenosine, and act in concert with other important neuromodulatory systems including dopamine, glutamate, and hypocretin.

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Section: Adenosine Receptor Heteromers and Receptor-receptor Interactmentioning

confidence: 55%

Sleep Homeostasis, Metabolism, and Adenosine

Holst

Landolt

2015

Curr Sleep Medicine Rep

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“…The mGluR5 are primarily expressed on post-synaptic neurons and glia cells and contribute importantly to long-term depression (Izumi et al 2012), but also to long-term potentiation. It was recently found that sleep loss increases mGluR5 availability in the human brain, and this increase was closely correlated with increased sleepiness after a night without sleep (Hefti et al 2013).…”

Section: Discussionmentioning

confidence: 96%

Adenosine, Caffeine, and Performance: From Cognitive Neuroscience of Sleep to Sleep Pharmacogenetics

Urry

Landolt

2014

Current Topics in Behavioral Neurosciences

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An intricate interplay between circadian and sleep-wake homeostatic processes regulate cognitive performance on specific tasks, and individual differences in circadian preference and sleep pressure may contribute to individual differences in distinct neurocognitive functions. Attentional performance appears to be particularly sensitive to time of day modulations and the effects of sleep deprivation. Consistent with the notion that the neuromodulator, adenosine adenosine , plays an important role in regulating sleep pressure, pharmacologic and genetic data in animals and humans demonstrate that differences in adenosinergic tone affect sleepiness, arousal and vigilant attention attention in rested and sleep-deprived states. Caffeine Caffeine -the most often consumed stimulant in the world-blocks adenosine receptors and normally attenuates the consequences of sleep deprivation on arousal, vigilance, and attention. Nevertheless, caffeine cannot substitute for sleep, and is virtually ineffective in mitigating the impact of severe sleep loss on higher-order cognitive functions. Thus, the available evidence suggests that adenosinergic mechanisms, in particular adenosine A2A receptor-mediated signal transduction, contribute to waking-induced impairments of attentional processes, whereas additional mechanisms must be involved in higher-order cognitive consequences of sleep deprivation. Future investigations should further clarify the exact types of cognitive processes affected by inappropriate sleep. This research will aid in the quest to better understand the role of different brain systems (e.g., adenosine and adenosine receptors) in regulating sleep, and sleep-related subjective state, and cognitive processes. Furthermore, it will provide more detail on the underlying mechanisms of the detrimental effects of extended wakefulness, as well as lead to the development of effective, evidence-based countermeasures against the health consequences of circadian misalignment and chronic sleep restriction. In press (accepted): January 14, 2014 Addresses for correspondence:Hans-Peter Landolt, Ph.D.

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“…Eighty-two healthy right-handed volunteers (12 females) between 19 and 35 years completed the sleep deprivation experiment (see refs 30,59, for further details on the study protocols). All volunteers reported to be good sleepers, adhere to regular bedtimes, be in good physical health, and have no history of neurological or psychiatric disorders.…”

Section: Methodsmentioning

confidence: 99%

Functional Polymorphisms in Dopaminergic Genes Modulate Neurobehavioral and Neurophysiological Consequences of Sleep Deprivation

Holst

Müller

Valomon

et al. 2017

Sci Rep

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Sleep deprivation impairs cognitive performance and reliably alters brain activation in wakefulness and sleep. Nevertheless, the molecular regulators of prolonged wakefulness remain poorly understood. Evidence from genetic, behavioral, pharmacologic and imaging studies suggest that dopaminergic signaling contributes to the behavioral and electroencephalographic (EEG) consequences of sleep loss, although direct human evidence thereof is missing. We tested whether dopamine neurotransmission regulate sustained attention and evolution of EEG power during prolonged wakefulness. Here, we studied the effects of functional genetic variation in the dopamine transporter (DAT1) and the dopamine D2 receptor (DRD2) genes, on psychomotor performance and standardized waking EEG oscillations during 40 hours of wakefulness in 64 to 82 healthy volunteers. Sleep deprivation consistently enhanced sleepiness, lapses of attention and the theta-to-alpha power ratio (TAR) in the waking EEG. Importantly, DAT1 and DRD2 genotypes distinctly modulated sleep loss-induced changes in subjective sleepiness, PVT lapses and TAR, according to inverted U-shaped relationships. Together, the data suggest that genetically determined differences in DAT1 and DRD2 expression modulate functional consequences of sleep deprivation, supporting the hypothesis that striato-thalamo-cortical dopaminergic pathways modulate the neurobehavioral and neurophysiological consequences of sleep loss in humans.

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Increased Metabotropic Glutamate Receptor Subtype 5 Availability in Human Brain After One Night Without Sleep

Cited by 86 publications

References 55 publications

Sleep Homeostasis, Metabolism, and Adenosine

Sleep Homeostasis, Metabolism, and Adenosine

Adenosine, Caffeine, and Performance: From Cognitive Neuroscience of Sleep to Sleep Pharmacogenetics

Functional Polymorphisms in Dopaminergic Genes Modulate Neurobehavioral and Neurophysiological Consequences of Sleep Deprivation

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