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

Abstract

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.

Caffeine Use among Active Duty Navy and Marine Corps Personnel

“…Adenosine is a neuromodulator that acts as a regulator of sleep and arousal [59,60]. Caffeine competes with adenosine at adenosine receptor sites to increase arousal and reduce the propensity to sleep [60,61]. Experimental studies indicate that caffeine can reduce sleep duration, likely in relation to the dosage and proximity to bedtime.…”

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“…; Cunha and Agostinho ; Lara ; Chen and Chern ; Porciúncula et al . ; Urry and Landolt ; Nehlig ). In fact, the main molecular mechanism of action established for non‐toxic doses of caffeine is the antagonism (not the agonism) of adenosine receptors (Fredholm et al .…”

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“…However, these are not the only chemical mediators in this regard, and norepinephrine, serotonin, histamine, orexin, dopamine, and melatonin are some neurotransmitters that regulate and stabilize the sleep-wake cycle (5,6). Additionally, adenosine, affecting the pre-optic area, sets off sleep (6,7). While mediators associated with immunity, such as interleukin beta 1 and tumor necrotizing factor (TNF), facilitate non-REM sleep in physiological conditions (8).…”