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Robert E. Strecker

Researcher at VA Boston Healthcare System

Publications -  131
Citations -  11114

Robert E. Strecker is an academic researcher from VA Boston Healthcare System. The author has contributed to research in topics: Sleep deprivation & Basal forebrain. The author has an hindex of 49, co-authored 128 publications receiving 10201 citations. Previous affiliations of Robert E. Strecker include Princeton University & Harvard University.

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Adenosine: a mediator of the sleep-inducing effects of prolonged wakefulness.

TL;DR: The data reported here suggest that the major criteria for a neural sleep factor mediating the somnogenic effects of prolonged wakefulness are satisfied by adenosine, a neuromodulator whose extracellular concentration increases with brain metabolism and which, in vitro, inhibits basal forebrain cholinergic neurons.
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Control of Sleep and Wakefulness

TL;DR: Genetic studies suggest that brain mechanisms controlling waking and NREM sleep are strongly conserved throughout evolution, underscoring their enormous importance for brain function.
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Adenosine and sleep–wake regulation

TL;DR: Evidence indicates that a cascade of signal transduction induced by basal forebrain adenosine A1 receptor activation in cholinergic neurons leads to increased transcription of the A1 receptors, which may play a role in mediating the longer-term effects of sleep deprivation.
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Brain site-specificity of extracellular adenosine concentration changes during sleep deprivation and spontaneous sleep: an in vivo microdialysis study.

TL;DR: The unique pattern of sleep-related changes in basal forebrain adenosine level lends strong support to the hypothesis that the sleep-promoting effects of adenosines, as well as the sleepiness associated with prolonged wakefulness, are both mediated by adenosinergic inhibition of a cortically projecting basal fore brain arousal system.
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Adenosinergic modulation of basal forebrain and preoptic/anterior hypothalamic neuronal activity in the control of behavioral state

TL;DR: A growing body of evidence supports the role of AD as a mediator of the sleepiness following prolonged wakefulness, a role in which its inhibitory actions on the BF wakefulness-promoting neurons may be especially important.