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

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology Vol. 278; no. 4; pp. 1048 - R1056
• Main Authors: Ribeiro, Ana Cristina, Gilligan, John G, Kapas, Levente
• Format: Journal Article
• Language: English
• Published: United States 01.04.2000
• Subjects: Animals; Electroencephalography; Electromyography; Enzyme Inhibitors - pharmacology; Fourier Analysis; Homeostasis - physiology; Male; NG-Nitroarginine Methyl Ester - pharmacology; Nitric Oxide Synthase - antagonists & inhibitors; Nitric Oxide Synthase - metabolism; Rats; Rats, Sprague-Dawley; Sleep - drug effects; Sleep - physiology; Sleep Deprivation - enzymology; Sleep, REM - drug effects; Sleep, REM - physiology; Wakefulness - physiology
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.2000.278.4.r1048

Department of Biological Sciences, Fordham University, Bronx, New York 10458 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 of an NO synthase inhibitor, N -nitro- L -arginine methyl ester ( L -NAME, a cumulative dose of 100 mg/kg). Amounts and intensity of sleep were increased in response to 8 h of SD in control rats ( n  = 8). Sleep amounts remained above baseline for 16 h after SD followed by a negative rebound. Rapid eye movement sleep (REMS) and non-REMS (NREMS) intensities were elevated for 16 and 4 h, respectively. L -NAME treatment ( n  = 8) suppressed the rebound increases in NREMS amount and intensity. REMS rebound was attenuated by L -NAME 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 rebound increases in NREMS suggests that NO may play a role as a signaling molecule in homeostatic regulation of NREMS. rapid eye movement sleep; fast Fourier analysis; N -nitro- L -arginine methyl ester; electroencephalography; slow-wave activity