Kapás L, Krueger J M
Department of Physiology and Biophysics, University of Tennessee, Memphis 38163, USA.
Brain Res Bull. 1996;41(5):293-8. doi: 10.1016/s0361-9230(96)00227-4.
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 intra-cerebroventricularly with the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 400 micrograms) or molsidomine (SIN-1, 7 and 70 micrograms). Seven micrograms of SIN-1 did not affect sleep, but increased the delta wave activity of the electroencephalogram (EEG) during nonrapid-eye-movement sleep (NREMS) and suppressed EEG alpha and beta activities in NREMS and delta, theta, and beta activities during wakefulness. Seventy micrograms of SIN-1 significantly increased NREMS after a latency of approximately 9 h. EEG power was suppressed in each frequency band during rapid-eye-movement sleep (REMS) and wakefulness, whereas during NREMS, delta activities were increased after the injection of 7 micrograms 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 accompanied the sleep changes. The EEG theta, alpha, and beta activities were suppressed in both wakefulness and REMS. Collectively, these results are consistent with the hypothesis that NO plays a role in the regulation of vigilance.
