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. Author manuscript; available in PMC: 2008 Jan 1.
Published in final edited form as: Neurosci Biobehav Rev. 2007 Mar 12;31(5):775–824. doi: 10.1016/j.neubiorev.2007.02.004

Figure 4.

Figure 4

The schematic of human brain depicting regions that are involved in the generation and maintenance slow-wave sleep (SWS). Following initiation of sleep, suppressed neuronal activity in the wake-promoting regions of the brain allow for the activation of γ-aminobutyric acid (GABA) and Galanin (Gal) synthesizing cells in the anterior hypothalamus/preoptic area (AH/POA). Increased activity of GABA and Galanin synthesizing cells in the AH/POA (red) ultimately generates slow wave sleep (SWS). Those GABA and Galanin synthesizing cells innervate the major wake-promoting cell groups of the brain including: histaminergic cells (HA) in the tuberomammilary nucleus (PH-TMN), hypocretin/orexinergic cells (Hcrt) in the lateral hypothalamus (LH), noradrenergic cells (NE) in the locus coeruleus (LC), serotonergic cells (5-HT) in the raphe nucleus (RN) and cholinergic cells (Ach) in the pedunculopontine tegmentum (PPT). The continued inhibition of these wake-promoting structures, via GABA and Galanin release, maintains episodes of SWS. Due to increased GABA and Galanin release, neuronal activity remains suppressed in other wake-promoting regions including: the medial prefrontal cortex (mPFC), suprachiasmatic nucleus (SCN), basal forebrain (BF), ventral tegmental area (VTA)/substantis nigra compacta (SNc) and medial reticular formation (MRF). In addition to AH/POA GABA and Galanin synthesizing cells, increased activity of GABAergic cells in layers I and II of the cortex and cells in the solitary nucleus also contribute to the maintenance of SWS.