SLEEP-DEPRIVATION REDUCES THE CITALOPRAM-INDUCED INHIBITION OF SEROTONINERGIC NEURONAL FIRING IN THE NUCLEUS RAPHE DORSALIS OF THE RAT

Sleep deprivation (SD) for one night induces mood improvement in depre ssed patients. However, relapse often occurs on the day after deprivat ion subsequently to a sleep episode. In light of the possible involvem ent of central serotonin (5-hydroxytryptamine, 5-HT) neurotransmission in both depression and sleep mechanisms, we presently investigated, i n the rat, the effects of SD and recovery sleep on the electrophysiolo gical response of 5-HT neurons in the nucleus raphe dorsalis (NRD) to an acute challenge with the 5-HT reuptake blocker citalopram. In all r ats, citalopram induced a dose-dependent inhibition of the firing of N RD neurons recorded under chloral hydrate anaesthesia. After SD, achie ved by placing rats in a slowly rotating cylinder for 24 h, the inhibi tory action of citalopram was significantly reduced (with a concomitan t 53% increase in its ED(50) value). After a recovery period of 4 h, a normal susceptibility of the firing to citalopram was restored. The d ecreased sensitivity of 5-HT neuronal firing to the inhibitory effect of citalopram after SD probably results in an enhancement of 5-HT neur otransmission. Such an adaptive phenomenon (similar to that reported a fter chronic antidepressant treatment), and its normalization after re covery sleep, parallel the mood improvement effect of SD and the subse quent relapse observed in depressed patients. These data suggest that the associated changes in 5-HT autocontrol of the firing of NRD seroto ninergic neurons are relevant to the antidepressant action of SD.