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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
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