Article ID Journal Published Year Pages File Type
5737020 Current Opinion in Neurobiology 2017 8 Pages PDF
Abstract

•Cholinergic, GABA and glutamatergic neurons all affect cortical activation.•Cholinergic neurons suppress cortical delta activity and promote cortical plasticity.•GABA/parvalbumin neurons promote gamma activity and fast arousals from sleep.•GABA/somatostatin neurons inhibit wake-promoting neurons.•Increases in extracellular adenosine promote sleep during prolonged wakefulness.

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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