LESION OF DESCENDING 5-HT PATHWAYS INCREASES ZIMELDINE-INDUCED WAKINGIN RATS

Sleep, waking, and EEG power spectra were investigated in rats with sp inal 5,6-dihydroxytryptamine (5,6-DHT) lesions, following 20 mg/kg zim eldine or vehicle IP injections. 5,6-DHT selectively lesioned the desc ending serotonergic pathways. Lesion alone did not change sleep and wa king stages compared to baseline, except for a reduction in REM sleep. Consistent with earlier findings, zimeldine in nonlesioned rats incre ased waking the first 2 h of recording. Zimeldine treatment in lesione d rats gave a significant additional 50% increase in waking the first 2 h and a corresponding decrease in total slow wave sleep, suggesting a potentiation of these effects. Zimeldine gave no significant changes in waking EEG power spectral density. Lesion gave a tendency to reduc tion between 4.0 and 15.5 Hz compared with baseline, and between 10.0 and 16.5 compared to the independent control group. In both comparison s, the combined treatment strengthened this effect, again suggesting a potentiating effect of lesion. In sleep, zimeldine reduced power over the whole spectrum (0.5-20.0 Hz), less in the lower frequencies than in the higher frequencies.