Endotoxin-induced reduction of social investigation by mice: interaction with amphetamine and anti-inflammatory drugs
| Autor: | Rod J. Fishkin, James T. Winslow |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Lipopolysaccharides
Male medicine.medical_specialty medicine.drug_class Anti-Inflammatory Agents Adrenergic Mice Internal medicine medicine Animals Drug Interactions Amphetamine Dexamethasone Sickness behavior Flavonoids Pharmacology Behavior Animal Dose-Response Relationship Drug biology business.industry Antagonist Dose–response relationship Endocrinology Exploratory Behavior biology.protein Corticosteroid Cyclooxygenase business medicine.drug |
| Zdroj: | Psychopharmacology. 132:335-341 |
| ISSN: | 1432-2072 0033-3158 |
| DOI: | 10.1007/s002130050353 |
| Popis: | Previous studies indicate that some aspects of endotoxin-induced sickness behavior in rats may be mediated by interleukin-1 stimulated events and can be attenuated by corticosteroids, cyclooxygenase inhibitors and the interleukin-1-receptor antagonist. In the current studies, we replicate and extend these findings in adult male mice. A relatively low dose of lipopolysaccharide (LPS; 15 micrograms/kg, IP) was used to reliably induce a 50-60% reduction in the social investigation of a juvenile conspecific at 2-3 h after injection. Amphetamine (2.0-4.0 mg/kg, IP, 30 min pre-LPS) exacerbated LPS-induced decreases in investigation. Administration of methylprednisolone (10-30 mg/kg, IP), indomethacin (3-30 mg/kg, IP), and ibuprofen (1-100 mg/kg, IP) 1 h before LPS significantly reduced LPS-induced sickness behavior at several doses. Dexamethasone (0.1-10 mg/kg, IP) partially antagonized sickness. Representative flavonoids rohitukine (0.01-100.0 mg/kg, IP) and chrysin (0.01-10 mg/kg, IP) also antagonized LPS-induced deficits in social investigation. These studies replicate and extend previous studies in rat to demonstrate systematic effects of low doses of LPS, antagonism by anti-inflammatory drugs and enhancement of LPS effects by amphetamine. The latter findings are consistent with a modulatory role for adrenergic activation on interleukin-1 release stimulated by endotoxicity. |
| Databáze: | OpenAIRE |
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