Journal
CURRENT OPINION IN NEUROBIOLOGY
Volume 44, Issue -, Pages 159-166Publisher
CURRENT BIOLOGY LTD
DOI: 10.1016/j.conb.2017.05.004
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Funding
- US Veterans Administration [I01BX001356]
- National Institutes of Mental Health [R03 MH107650, R01 MH039683]
- National Institute of Neurological Disorders and Stroke [R21 NS093000]
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The diverse cell-types of the basal forebrain control sleep wake states, cortical activity and reward processing. Large, slow-firing, cholinergic neurons suppress cortical delta activity and promote cortical plasticity in response to reinforcers. Large, fast-firing, cortically-projecting GABAergic neurons promote wakefulness and fast cortical activity. In particular, parvalbumin/GABAergic neurons promote neocortical gamma band activity. Conversely, excitation of slower-firing somatostatin/GABAergic neurons promotes sleep through inhibition of cortically-projecting neurons. Activation of glutamatergic neurons promotes wakefulness, likely by exciting other cortically-projecting neurons. Similarly, cholinergic neurons indirectly promote wakefulness by excitation of wake-promoting, cortically-projecting GABAergic neurons and/or inhibition of sleep-promoting somatostatin/GABAergic neurons. Both glia and neurons increase the levels of adenosine during prolonged wakefulness. Adenosine presynaptically inhibits glutamatergic inputs to wake promoting cholinergic and GABAergic/parvalbumin neurons, promoting sleep.
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