Reduced Neurobehavioral Impairment from Sleep Deprivation in Older Adults: Contribution of Adenosinergic Mechanisms

Abstract

A night without sleep is followed by enhanced sleepiness, increased low-frequency activity in the waking EEG, and reduced vigilant attention. The magnitude of these changes is highly variable among healthy individuals. Findings in young men of low and high subjective caffeine sensitivity suggest that adenosinergic mechanisms contribute to inter-individual differences in sleep deprivation-induced changes in EEG theta activity, as well as optimal performance on the psychomotor vigilance task (PVT). In comparison to young subjects, healthy adults of older age typically feel less sleepy after sleep deprivation, and show fewer response lapses, and faster reaction times on the PVT, especially in the morning after the night without sleep. We hypothesized that age-related changes in adenosine signal transmission underlie reduced vulnerability to sleep deprivation in older individuals. To test this hypothesis, the combined effects of prolonged wakefulness and the adenosine receptor antagonist, caffeine, on an antero-posterior power gradient in EEG theta activity and PVT performance were analyzed in healthy older and caffeine-insensitive and -sensitive young men. The results show that age-related differences in sleep loss-induced changes in brain rhythmic activity and neurobehavioral functions are mirrored in young individuals of low and high sensitivity to the stimulant effects of caffeine. Moreover, the effects of sleep deprivation and caffeine on regional theta power and vigilant attention are inversely correlated across older and young age groups. Genetic variants of the adenosine A2A receptor gene contribute to individual differences in neurobehavioral performance in rested and sleep deprived state, and modulate the actions of caffeine in wakefulness and sleep. Based upon this evidence, we propose that age-related differences in A2A receptor-mediated signal transduction could be involved in age-related changes in the vulnerability to acute sleep deprivation.

Preeclampsia and the brain: neural control of cardiovascular changes during pregnancy and neurological outcomes of preeclampsia

“…Synaptic release of norepinephrine activates astrocytic α 2 -adrenoreceptors, which triggers the extracellular release of ATP, that is then hydrolyzed to adenosine (196, 219, 220). The adenosine binds to presynaptic A1Rs and induces hyperpolarization by inactivating Ca 2+ inward channels and activating K + channels (196, 221). Studies employing SHRs observed increased A1R expression in the NTS (194, 222), with enhanced sensitivity to adenosine (222) that blunted BRS resulting in a hypertensive state (193, 196, 223, 224).…”

A Unified Model of Performance for Predicting the Effects of Sleep and Caffeine

“…Raw data were available for all studies except study V4, for which group-average data were captured from a published figure. 8 …”

“…Subjects received a capsule with either placebo after 11 and 23 h of wakefulness (at 19:00 and 07:00, respectively) or 200 mg of caffeine on each of the two occasions. 8,15 The TSD phase was preceded by 2 nights of 8 h TIB (baseline) and followed by 1 night of 10.5 h TIB (recovery). During the TSD phase, subjects completed 14 sessions of a 10-min PVT at 3-h intervals.…”

Principal component scoring of the resting EEG spectrum provides further evidence for age-associated disinhibition of the wake drive

“…On the other hand, it was recently shown that the process of normal aging can bring some advantages to older people living in modern 24-hour societies. For instance, they may better tolerate sleep deprivation compared to younger people [30][31][32][33]. It seems that research into ageassociated changes in principal component structure of the wake and sleep EEG signal can provide deeper insights into the regulatory processes underlying optimal sleep of older people, and their predisposition to both certain sleep disturbances and advantageous waking ability.…”