title: Salicylate as a partial inhibitor of emotional fever and body weight set-point in rats: behavioral and neuroendocrine study.
abstract: In this article, we report findings from behavioral and neuroendocrine experiments in rats under pharmacologically induced antipyretic conditions. Endpoints included emotional fever, body weight setpoint, and in situ corticotropin-releasing hormone mRNA (CRHmRNA) expression. Nine male Wistar rats were treated with acetylsalicylic acid (ASA) 0.04 g/kg ip in vehicle. On alternating days, all rats received saline (0.9% w/v) as a control. ASA was selected chiefly for its antipyretic and also for effects on metabolism. It has been demonstrated that gentle handling affects body weight and body temperature in rats. In Experiment 1, we investigated whether blocking emotional fever by ASA treatment would inhibit the lowering of the body weight setpoint induced by handling of the rats. Rats were exposed to a daily food-hoarding session under handling stress, and their body weight setpoints were calculated from the hoarding measurements. As rats received ASA and saline in an alternating manner, two setpoints were calculated. In Experiment 2, we performed neuroendocrine analyses of CRHmRNA expression in the same group of animals from Experiment 1. CRHmRNA was determined by in situ hybridization. Results indicated that ASA treatment in rats significantly decreased the body weight setpoint (P=.02) and significantly prevented increases in body temperature due to emotional fever (P=.03) when compared to their control values. Findings also revealed that hypothalamic CRH expression was increased when rats were treated with ASA. ASA did partially block fever induced by handling, but it is difficult to confirm whether emotion was also inhibited by treatment. Taken together, these results indicate that salicylates affect energy balance and might be a good inhibitor of body weight gain in rats.
authors.affiliation: Département de Physiologie, Faculté de Médecine, Université Laval, Quebec, Canada G1K 7P4.
authors.forename: C
authors.initials: C
authors.lastname: Michel
authors.forename: P
authors.initials: P
authors.lastname: Frankham
authors.forename: M
authors.initials: M
authors.lastname: Cabanac
mesh_terms: D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000494:pharmacology* / Q000627:therapeutic use; D001241:Aspirin / Q000494:pharmacology* / Q000627:therapeutic use; D001831:Body Temperature / Q000187:drug effects* / Q000502:physiology; D001835:Body Weight / Q000187:drug effects* / Q000502:physiology; D003346:Corticotropin-Releasing Hormone / Q000187:drug effects / Q000235:genetics; D004644:Emotions / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects; D005334:Fever / Q000188:drug therapy / Q000523:psychology; D006234:Handling, Psychological; D008297:Male; D010286:Paraventricular Hypothalamic Nucleus / Q000187:drug effects / Q000378:metabolism; D012333:RNA, Messenger / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D013312:Stress, Physiological / Q000378:metabolism*; D013315:Stress, Psychological / Q000378:metabolism
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D012333:RNA, Messenger; D003346:Corticotropin-Releasing Hormone; D001241:Aspirin