NITRIC-OXIDE DONORS SIN-1 AND SNAP PROMOTE NONRAPID-EYE-MOVEMENT SLEEP IN RATS

We previously showed that inhibition of brain NO production suppresses sleep in rats and rabbits. In the present experiments we studied the effects of stimulation of NO-receptive brain mechanisms on sleep, Male rats were injected intracerebroventricularly with the NO donor S-nitr oso-N-acetylpenicillamine (SNAP, 400 mu g) or molsidomine (SIN-1, 7 an d 70 mu g). Seven micrograms of SIN-1 did not affect sleep, but increa sed the delta wave activity of the electroencephalogram (EEG) during n onrapid-eye-movement sleep (NREMS) and suppressed EEG alpha and beta a ctivities in NREMS and delta, theta, and beta activities during wakefu lness, Seventy micrograms of SIN-1 significantly increased NREMS after a latency of similar to 9 h. EEG power was suppressed in each frequen cy band during rapid-eye-movement sleep (REMS) and wakefulness, wherea s during NREMS, delta activities were increased after the injection of 7 mu g SIN-1, and higher frequencies were suppressed after both doses . On the recovery day sleep remained elevated, but EEG power returned to baseline. The effects of SNAP on NREMS were similar to those of SIN -1, but REMS was decreased and slight increases in brain temperature a ccompanied the sleep changes, The EEG theta, alpha, and beta activitie s were suppressed in both wakefulness and REMS. Collectively, these re sults are consistent with the hypothesis that NO plays a role in the r egulation of vigilance.