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. Author manuscript; available in PMC: 2009 Feb 20.
Published in final edited form as: Eur J Neurosci. 2006 Mar;23(5):1301–1310. doi: 10.1111/j.1460-9568.2006.04652.x

Figure 6.

Figure 6

Proposed model to explain why lesions of the preoptic area (POA) reduce sleep bout durations but lengthen wake bout durations. Arrows depict known excitatory (+) and inhibitory (−) connections between the POA and the wake-promoting basal forebrain (BF), tuberomammillary nucleus (TMN), and mesopontine wake-promoting neurons (e.g., in locus coeruleus and dorsal raphe); reciprocal connections between these regions are not shown. According to this model, POA lesions reduce sleep bout durations by destroying sleep-promoting neurons in that region. The lengthening of wake bout durations arise from (1) the removal of direct GABAergic inhibition of the BF and (2) the removal of GABAergic inhibition of the TMN, thereby producing increased histaminergic excitatory input to the BF. In this way, wake-promoting mesopontine neurons are activated due to increased excitation from the BF and decreased inhibition from the POA.