Skip to main content
. Author manuscript; available in PMC: 2011 Dec 22.
Published in final edited form as: Neuron. 2010 Dec 22;68(6):1023–1042. doi: 10.1016/j.neuron.2010.11.032

Figure 1. The wake-sleep switch.

Figure 1

Many wake-promoting projections arise from neurons in the upper brainstem (A). Cholinergic neurons (aqua) provide the major input to the thalamus, whereas monoaminergic and (presumably) glutamatergic neurons (dark green) provide direct innervation of the the hypothalamus. basal forebrain, and cerebral cortex. The orexin neurons in the lateral hypothalamus (blue) reinforce activity in these brainstem arousal pathways and also directly excite the cerebral cortex and BF. The main sleep-promoting pathways (magenta in B) from the ventrolateral (VLPO) and median (MnPO) preoptic nuclei inhibit the components of the ascending arousal pathways in both the hypothalamus and the brainstem (pathways that are inhibited are shown as open circles and dashed lines). However, the ascending arousal systems are also capable of inhibiting the VLPO (C). This mutually inhibitory relationship of the arousal- and sleep-promoting pathways produces the conditions for a “flip-flop” switch, which can generate rapid and complete transitions between waking and sleeping states. Abbreviations: DR, dorsal raphe nucleus (serotonin); LC, locus coeruleus (norepinephrine); LDT, laterodorsal tegmental nucleus (acetylcholine); PB, parabrachial nucleus (glutamate); PC, precoeruleus area (glutamate); PPT, pedunculopontine tegmental nucleus (acetylcholine); TMN, tuberomammillary nucleus (histamine); vPAG, ventral periaqueductal gray (dopamine).