Nitric oxide modulates the discharge rate of basal forebrain neurones: a study in freely moving rats.

In urethane-anaesthetized rats the infusion of a nitric oxide (NO)-donor [NOC-18, 1 mM (DETA/NO); 2,2'-(hydroxynitrosohydrazino)bis-ethanamine)] into the basal forebrain (BF) inhibited the discharge rate of most neurones, suggesting that NO may promote sleep via inhibition of wake-promoting neurones in the BF. However, this hypothesis still needs to be confirmed in freely moving rats. The objective of this study was to examine whether NO modulates the discharge rate of BF neurones in freely moving rats in a similar manner to anaesthetized rats. We measured the discharge rates of BF neurones in freely moving rats during microdialysis infusion of a NO-donor (1 mm; NOC-18) in different vigilance states. Neurones were characterized as wake (W)-on (51.8%), W-off (28.6%) and W/non-rapid eye movement (REM)-independent (21.4%) based on their discharge profiles during wakefulness (W) and non-REM sleep. The NO-donor affected the discharge rate of most BF neurones during quiet wakefulness (QW; 55%) and non-REM sleep (64%). The most prominent response in all neuronal groups was a decrease in the discharge rate during QW and non-REM sleep. A small subpopulation of neurones increased the discharge rate. The increase in NO in the BF during prolonged wakefulness may facilitate sleep via inhibition of wake-promoting neurones.