title: Restraint changes pentobarbital-induced sleeping time in rats: evidence that arousal is modulated by brain corticotropin-releasing hormone and opioid in stress.
abstract: The effect of restraint of different duration on sodium pentobarbital (PbNa)-induced sleeping time was examined in rats. 1 h-restraint significantly shortened PbNa (50 mg/kg b.wt., administered i.p. immediately after restraint)-induced sleeping time as reported previously, whereas 2 h-restraint significantly prolonged the sleeping time. Naloxone (1 mg/kg b.wt.) administered i.p. 15 min before the start of restraint further exaggerated the 1 h-restraint-caused shortening of PbNa-induced sleeping time, and it blocked the 2 h-restraint-caused prolongation of the sleeping time. SDZ202-250 (0.1 pmol and 0.5 pmol), a selective mu agonist, but not [D-Pen2-D-Pen5]enkephalin (0.1 pmol-1.0 nmol), a selective delta agonist, or U50488H (0.1 pmol-1.0 nmol), a selective kappa agonist, administered i.c.v. 15 min before the i.p. injection of PbNa significantly prolonged PbNa-induced sleeping time; its prolongation was blocked by naloxone. These results suggest that a mu receptor-binding opioid prolongs PbNa-induced sleeping time in stress. The 2 h-restraint-caused prolongation of PbNa-induced sleeping time was also blocked by alpha-helical CRH(9-41) (26 nmol), a corticotropin-releasing hormone (CRH) receptor antagonist, administered i.c.v. 15 min before the start of restraint. In conjunction with our previous findings that the i.c.v. administration of CRH shortens PbNa-induced sleeping time and the 1 h restraint-caused shortening of PbNa-induced sleeping time is blocked by the CRH receptor antagonist, the present results suggest that CRH may stimulate an opioid-specific sedative mechanism, thus causing the prolongation of PbNa-induced sleeping time in 2 h-restraint.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Medicine, Tokyo Women's Medical College, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Shibasaki
authors.forename: T
authors.initials: T
authors.lastname: Imaki
authors.forename: M
authors.initials: M
authors.lastname: Hotta
authors.forename: N
authors.initials: N
authors.lastname: Ling
authors.forename: H
authors.initials: H
authors.lastname: Demura
mesh_terms: D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D000700:Analgesics / Q000494:pharmacology; D000818:Animals; D001143:Arousal / Q000187:drug effects / Q000502:physiology*; D001921:Brain / Q000502:physiology* / Q000503:physiopathology; D002552:Cerebral Ventricles / Q000187:drug effects / Q000502:physiology; D003346:Corticotropin-Releasing Hormone / Q000008:administration & dosage / Q000494:pharmacology / Q000502:physiology*; D004723:Endorphins / Q000502:physiology*; D020881:Enkephalin, D-Penicillamine (2,5)-; D004745:Enkephalins / Q000008:administration & dosage / Q000494:pharmacology; D007276:Injections, Intraventricular; D008297:Male; D009020:Morphine / Q000008:administration & dosage / Q000494:pharmacology; D010424:Pentobarbital / Q000494:pharmacology*; D010446:Peptide Fragments / Q000008:administration & dosage / Q000494:pharmacology; D011759:Pyrrolidines / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017450:Receptors, Opioid, mu / Q000502:physiology*; D012149:Restraint, Physical; D012890:Sleep / Q000187:drug effects / Q000502:physiology*; D013315:Stress, Psychological / Q000503:physiopathology*
chemical_list: D000700:Analgesics; D004723:Endorphins; D004745:Enkephalins; D010446:Peptide Fragments; D011759:Pyrrolidines; D017450:Receptors, Opioid, mu; D019900:3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer; D009020:Morphine; D020881:Enkephalin, D-Penicillamine (2,5)-; D003346:Corticotropin-Releasing Hormone; C045089:corticotropin releasing hormone (9-41); D010424:Pentobarbital