L-364,718, a cholecystokinin-A receptor antagonist, suppresses feeding-induced sleep in rats

• Published in: American journal of physiology. Regulatory, integrative and comparative physiology integrative and comparative physiology, 2001-05, Vol.280 (5), p.1420-R1426
• Main Authors: Shemyakin, Alexei, Kapas, Levente
• Format: Article
• Language: English
• Subjects: Animals; Body Weight; Devazepide - administration & dosage; Devazepide - pharmacology; Eating - physiology; Electroencephalography - drug effects; Electromyography - drug effects; Feeding Behavior - physiology; Food Deprivation; Injections, Intraperitoneal; Male; Rats; Rats, Sprague-Dawley; Receptor, Cholecystokinin A; Receptors, Cholecystokinin - antagonists & inhibitors; Reference Values; Sleep - drug effects; Sleep - physiology; Sleep Stages - drug effects; Sleep Stages - physiology; Sleep, REM - drug effects; Sleep, REM - physiology
• ISSN: 0363-6119; 1522-1490
• DOI: 10.1152/ajpregu.2001.280.5.R1420

Department of Biological Sciences, Fordham University, Bronx, New York 10458 Feeding induces increased sleep in several species, including rats. The aim of the study was to determine if CCK plays a role in sleep responses to feeding. We induced excess eating in rats by 4 days of starvation and studied the sleep responses to refeeding in control and CCK-A receptor antagonist-treated animals. Sleep was recorded on 2 baseline days when food was provided ad libitum. After the starvation period, sleep was recorded on 2 refeeding days when the control rats ( n  = 8) were injected with vehicle and the experimental animals ( n  = 8) received intraperitoneal injections of L-364,718 (500 µg/kg, on both refeeding days). In the control group, refeeding caused increases in rapid eye movement sleep (REMS) and non-REMS (NREMS) and decreases in NREMS intensity as indicated by the slow-wave activity (SWA) of the electroencephalogram. CCK-A receptor antagonist treatment completely prevented the SWA responses and delayed the NREMS responses to refeeding; REMS responses were not simply abolished, but the amount of REMS was below baseline after the antagonist treatment. These results suggest that endogenous CCK, acting on CCK-A receptors, may play a key role in eliciting postprandial sleep. electroencephalogram slow-wave activity; food intake; brain temperature; food deprivation; non-rapid eye movement sleep