title: Repeated Cold Stress Enhances the Acute Restraint Stress-Induced Hyperthermia in Mice.
abstract: The rodents exposed to repeated cold stress according to a specific schedule, known as specific alternation of rhythm in temperature (SART), exhibit autonomic imbalance, and is now used as an experimental model of fibromyalgia. To explore the susceptibility of SART-stressed animals to novel acute stress, we tested whether exposure of mice to SART stress for 1 week alters the extent of acute restraint stress-induced hyperthermia. Mice were subjected to 7-d SART stress sessions; i.e., the mice were alternately exposed to 24 and 4°C at 1-h intervals during the daytime (09:00-16:00) and kept at 4°C overnight (16:00-09:00). SART-stressed and unstressed mice were exposed to acute restraint stress for 20-60 min, during which rectal temperature was monitored. Serum corticosterone levels were measured before and after 60-min exposure to restraint stress. SART stress itself did not alter the body temperature or serum corticosterone levels in mice. Acute restraint stress increased the body temperature and serum corticosterone levels, both responses being greater in SART-stressed mice than unstressed mice. The enhanced hyperthermic responses to acute restraint stress in SART-stressed mice were significantly attenuated by SR59230A, a β3adrenoceptor antagonist, but unaffected by diazepam, an anxiolytic, mifepristone, a glucocorticoid receptor antagonist, or indomethacin, a cyclooxygenase inhibitor. These results suggest that SART stress enhances the susceptibility of mice to acute restraint stress, characterized by increased hyperthermia and corticosterone secretion, and that the increased hyperthermic responses to acute stress might involve accelerated activation of sympathetic β3adrenoceptors, known to regulate non-shivering thermogenesis in the brown adipose tissue.
authors.affiliation: Faculty of Pharmacy, Kindai University.
authors.forename: Tomoyoshi
authors.initials: T
authors.lastname: Miyamoto
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Funakami
authors.forename: Erika
authors.initials: E
authors.lastname: Kawashita
authors.forename: Ai
authors.initials: A
authors.lastname: Nomura
authors.forename: Nanako
authors.initials: N
authors.lastname: Sugimoto
authors.forename: Haruka
authors.initials: H
authors.lastname: Saeki
authors.forename: Maho
authors.initials: M
authors.lastname: Tsubota
authors.forename: Seiji
authors.initials: S
authors.lastname: Ichida
authors.forename: Atsufumi
authors.initials: A
authors.lastname: Kawabata
mesh_terms: D002001:Adipose Tissue, Brown; D058673:Adrenergic beta-3 Receptor Antagonists; D000818:Animals; D014151:Anti-Anxiety Agents / Q000494:pharmacology; D003080:Cold Temperature; D003345:Corticosterone / Q000097:blood; D003975:Diazepam / Q000494:pharmacology; D005334:Fever / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D008297:Male; D051379:Mice; D015735:Mifepristone / Q000494:pharmacology; D011412:Propanolamines / Q000494:pharmacology; D011965:Receptors, Glucocorticoid / Q000037:antagonists & inhibitors; D012149:Restraint, Physical; D013312:Stress, Physiological; D013315:Stress, Psychological / Q000097:blood / Q000188:drug therapy / Q000378:metabolism; D000071256:Uncoupling Protein 1 / Q000378:metabolism
chemical_list: C097869:3-(2-ethylphenoxy)-1-(1,2,3,4-tetrahydronaphth-1-ylamino)-2-propanol oxalate; D058673:Adrenergic beta-3 Receptor Antagonists; D014151:Anti-Anxiety Agents; D011412:Propanolamines; D011965:Receptors, Glucocorticoid; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1; D015735:Mifepristone; D003975:Diazepam; D003345:Corticosterone