Figure 4.
Sleep homeostasis in sleep-promoting effects of alcohol. A single dose (3 g/kg; intragastric) of alcohol, administered at the onset of the circadian active period, inhibits wake-promoting cholinergic neurons of the BF (Panel A & B) to promote NREM sleep as shown by a significant reduction in sleep onset latency (inset in Panel C) coupled with a significant increase in the amount of time spent in NREM sleep (Panel C). However, blockade of AD A1R in the BF resulted in an attenuation of alcohol- induced sleep promotion (Panel D), whereas local, reverse microdialysis perfusion of pharmacological relevant doses of alcohol into the BF significantly increased extracellular AD in the BF (Panel E; inset describes AD chromatogram) implicating adenosinergic mechanisms in alcohol-induced sleep promotion [adapted from Sharma et al., 2010b and Thakkar et al., 2010]. Lastly, in contrast to sham controls, animals with a selective lesion of the BF cholinergic neurons displayed attenuated alcohol-induced sleep [Panel F; unpublished data]; *= p < 0.05.