The reductions in sweetened milk intake induced by interleukin-1 and endotoxin are not prevented by chronic antidepressant treatment.
Administration of interleukin-1 (IL-1) and endotoxin (lipopolysaccharide, LPS) to rodents can decrease food intake, a behavioral response resembling the diminution of appetite observed in human depression. IL-1 and LPS are known to affect cerebral neurotransmission involving norepinephrine and serotonin, both of which have been implicated in feeding behavior and in the pharmacotherapy of depression in man. The ability of chronic antidepressant treatment to attenuate LPS-induced depressed feeding in rats has been cited as evidence that cytokines may be involved in human depression. Thus, we studied the effects of chronic treatment with the tricyclic antidepressant, imipramine, and the novel antidepressant, venlafaxine, on the sweetened milk intake challenged with intraperitoneally injected IL-1 beta and LPS. Chronic (from 2 to 8 weeks) treatment of the mice with imipramine (10 mg/kg once or twice daily) or venlafaxine (10 and 20 mg/kg/day) did not significantly alter the decreases in milk intake in response to mIL-1 beta or LPS. In some experiments, chronic imipramine slightly decreased body weight and slightly increased milk intake, but not food pellet intake. Venlafaxine had none of these effects. Analysis of variance did not indicate any significant interactions between the antidepressant and IL-1 or LPS treatments. These results indicate that chronic treatment with antidepressants does not significantly alter the responses to IL-1 or LPS in the mouse sweetened milk model of sickness behavior.
Dunn
A J
AJ
Department of Pharmacology and Therapeutics, Louisiana State University Health Sciences Center, Shreveport, LA 71130-3932, USA. adunn@lsuhsc.edu
Swiergiel
A H
AH
D018759:Adrenergic Uptake Inhibitors / Q000494:pharmacology; D000818:Animals; D000928:Antidepressive Agents / Q000276:immunology / Q000494:pharmacology*; D001066:Appetite / Q000187:drug effects* / Q000276:immunology; D001835:Body Weight / Q000187:drug effects / Q000276:immunology; D001921:Brain / Q000187:drug effects / Q000276:immunology / Q000378:metabolism; D003511:Cyclohexanols / Q000494:pharmacology; D003863:Depression / Q000188:drug therapy / Q000276:immunology* / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D004334:Drug Administration Schedule; D004435:Eating / Q000187:drug effects* / Q000276:immunology; D007099:Imipramine / Q000494:pharmacology; D007375:Interleukin-1 / Q000276:immunology / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000276:immunology / Q000494:pharmacology; D008297:Male; D051379:Mice; D008892:Milk / Q000378:metabolism; D015213:Neuroimmunomodulation / Q000187:drug effects* / Q000502:physiology; D009638:Norepinephrine / Q000378:metabolism; D012701:Serotonin / Q000378:metabolism; D017367:Selective Serotonin Reuptake Inhibitors / Q000494:pharmacology; D000069470:Venlafaxine Hydrochloride
D018759:Adrenergic Uptake Inhibitors; D000928:Antidepressive Agents; D003511:Cyclohexanols; D007099:Imipramine; D007375:Interleukin-1; D008070:Lipopolysaccharides; D009638:Norepinephrine; D012701:Serotonin; D017367:Selective Serotonin Reuptake Inhibitors; D000069470:Venlafaxine Hydrochloride