Abstract
Stress exposure activates the autonomic nervous system and leads to a body temperature increase (stress-induced hyperthermia, SIH). On the other hand, an activation of the immune system in response to an infection leads to fever. Both processes increase body temperature, and the relation between SIH and infection-induced fever has been subject to debate. It is not clear whether SIH is a form of fever, or whether both processes are more or less distinct. We therefore examined the relation between SIH and infection-induced fever by looking at the effects of a GABA(A) receptor agonist (diazepam) and a prostaglandin-synthesis blocking drug (acetylsalicylic acid. aspirin) on both the SIH response and fever in rats and mice. The present Study shows that the benzodiazepine diazepam but not the prostaglandin-synthesis blocking drug aspirin dose-dependently attenuated the SIH response in both rats and mice. In contrast, aspirin reduced both LPS- and IL-1 beta induced fever, whereas diazepam had little effect on these fever states. Altogether, Our findings Support the hypothesis that stress-induced hyperthermia and infection-incluced fever are two distinct processes mediated largely by different neurobiological mechanisims. (C) 2009 Elsevier Inc. All rights reserved.
Original language | English |
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Pages (from-to) | 37-43 |
Number of pages | 7 |
Journal | Physiology & behavior |
Volume | 98 |
Issue number | 1-2 |
DOIs | |
Publication status | Published - 4 Aug 2009 |
Keywords
- Diazepam
- Aspirin
- LPS
- IL-1 beta
- Psychoneuroimmunology
- SYMPATHETIC PREMOTOR NEURONS
- PROSTAGLANDIN EP3 RECEPTOR
- SINGLY HOUSED MICE
- DORSOMEDIAL HYPOTHALAMUS
- BODY-TEMPERATURE
- PHARMACOLOGICAL VALIDATION
- THERMOREGULATORY FUNCTIONS
- AMBIENT-TEMPERATURE
- FEBRILE RESPONSES
- RESTRAINT STRESS