The menagerie of the basal forebrain: how many (neural) species are there, what do they look like, how do they behave and who talks to whom?. (June 2017)

• Record Type: Journal Article
• Authors: Yang, Chun; Thankachan, Stephen; McCarley, Robert W; Brown, Ritchie E
• Is Part Of: Current opinion in neurobiology. Volume 44(2017)
• Page Start: 159
• Page End: 166
• Publication Date: 2017-06
• Subjects: Neurobiology -- Periodicals; 573.8
• DOI: 10.1016/j.conb.2017.05.004
• Languages: English
• ISSNs: 0959-4388

Abstract

Highlights: 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. Abstract : 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.