Stimulation of A1 adenosine receptors mimics the electroencephalographic effects of sleep deprivation.
N6-Cyclopentyladenosine (CPA), an A1 adenosine receptor agonist, increased EEG slow-wave activity in nonREM sleep when administered either systemically (0.1-3 mg/kg) or intracerebroventricularly (3.5-10 micrograms) in the rat. The power spectrum of EEG changes (as calculated by Fourier analysis) matched that produced by total sleep deprivation in the rat. The effects of CPA on the nonREM-sleep EEG were dose-dependent. These findings suggest that adenosine is an endogenous mediator of sleep-deprivation induced increases in EEG slow-wave activity, and therefore that increased adenosine release is a concomitant of accumulation of sleep need and may be involved in homeostatic feedback control of sleep expression.
Department of Biological Sciences, Stanford University, CA 94305, USA.
J H
JH
Benington
S K
SK
Kodali
H C
HC
Heller
D000241:Adenosine / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000502:physiology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D004305:Dose-Response Relationship, Drug; D004569:Electroencephalography / Q000187:drug effects*; D005583:Fourier Analysis; D007276:Injections, Intraventricular; D008297:Male; D058906:Purinergic P1 Receptor Agonists; D051381:Rats; D017208:Rats, Wistar; D012892:Sleep Deprivation / Q000502:physiology*; D012895:Sleep, REM / Q000502:physiology
D058906:Purinergic P1 Receptor Agonists; C048599:N(6)-cyclopentyladenosine; D000241:Adenosine