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Mahesh M. Thakkar

Researcher at University of Missouri

Publications -  77
Citations -  5560

Mahesh M. Thakkar is an academic researcher from University of Missouri. The author has contributed to research in topics: Non-rapid eye movement sleep & Basal forebrain. The author has an hindex of 35, co-authored 70 publications receiving 5066 citations. Previous affiliations of Mahesh M. Thakkar include VA Boston Healthcare System & Veterans Health Administration.

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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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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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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.
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Role of adenosine in behavioral state modulation: A microdialysis study in the freely moving cat

TL;DR: The observation that local perfusion of adenosine into either the basal forebrain or the laterodorsal tegmental nucleus dramatically decreases wakefulness suggests that these areas might represent a major site of action of the xanthine stimulants found in coffee and tea.
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Hippocampal synaptic plasticity and spatial learning are impaired in a rat model of sleep fragmentation

TL;DR: The results suggest that sleep fragmentation negatively impacts spatial learning, and loss of N‐methyl‐d‐aspartate receptor‐dependent LTP in the hippocampal CA1 region may be one mechanism involved in this deficit.