• Bin-Jia Zhang, Shu-Rong Shao, Kosuke Aritake, Atsuko Takeuchi, Yoshihiro Urade, Zhi-Li Huang, Michael Lazarus, and Wei-Min Qu.
• State Key Laboratory of Medical Neurobiology, Department of Pharmacology, Institutes of Brain Science and the Collaborative Innovation Center for Brain Science, Shanghai Medical College of Fudan University, Shanghai 200032, China. Electronic address: 071101009@fudan.edu.cn.
• Neuroscience. 2017 Jan 6; 340: 258-267.

AbstractInterleukin-1β (IL-1β) and prostaglandin (PG) D2 are endogenous sleep-promoting substances. Since it was reported that a highly selective cyclooxygenase-2 (COX-2) inhibitor, NS398, completely inhibited IL-1β-induced sleep in rats, IL-1β-induced sleep had been believed to be mediated by prostanoids, most probably PGD2. However, in the present study, pretreatment of rats with NS398 (3mg/kg) did not suppress the 64.2% increased non-rapid eye movement (non-REM, NREM) sleep during infusion of IL-1β (10ng) for 6h in the nocturnal (active) period between 23:00 and 5:00 into the subarachnoid space of the PGD2-sensitive sleep-promoting zone of the basal forebrain. Meanwhile, IL-1β at doses of 1.7 and 5μg/kg also significantly increased NREM sleep for 6h after intraperitoneal injection at 20:00 (light-off time) by 76.8% and 121.1%, respectively, in wild-type (WT) mice, by 67.7% and 147.3%, respectively, in WT mice pretreated with NS398 (5mg/kg) and by 108.9% and 121.6%, respectively, in PGD2 receptor (DP1R) knockout mice. These results indicate that IL-1β-induced NREM sleep is independent of the PGD2/DP1R system and other COX-2-derived prostaglandins in rats and mice.Copyright © 2016 IBRO. Published by Elsevier Ltd. All rights reserved.

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