Systemic injection of a nitric oxide synthase inhibitor suppresses sleep responses to sleep deprivation in rats

We hypothesized that nitric oxide (NO) may play a role in homeostatic sleep regulation. To test this hypothesis, we studied the sleep deprivation (SD) -induced homeostatic sleep responses after intraperitoneal administration o f an NO synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME, a cumulative dose of 100 mg/kg). Amounts and intensity of sleep were increa sed in response to 8 h of SD in control rats (n = 8). Sleep amounts remaine d above baseline for 16 h after SD followed by a negative rebound. Rapid ey e movement sleep (REMS) and non-REMS (NREMS) intensities were elevated for 16 and 4 h, respectively. L-NAME treatment (n = 8) suppressed the rebound i ncreases in NREMS amount and intensity. REMS rebound was attenuated by L-NA ME in the first dark period after SD; however, a second rebound appeared in the subsequent dark period. REMS intensity did not increase after SD in L- NAME-injected rats. The finding that the NO synthase inhibitor suppressed r ebound increases in NREMS suggests that NO may play a role as a signaling m olecule in homeostatic regulation of NREMS.