Abstract

Introduction

Effects on CNS Neurotransmission

Effects on Feeding

References

Discussion
Board

Endotoxin (lipopolysaccharide, LPS) and interleukin-1 (IL-1) administration induce hypophagia in rodents. Both IL-1 and LPS are known to activate cerebral noradrenergic and serotonergic systems, and IL-1 affects histamine and acetylcholine. Each of these neurotransmitters has been implicated in feeding behavior. Therefore, the ability of specific antagonists of the above neurotransmitter systems to counteract feeding responses to peripherally injected mIL-1beta and LPS was studied. Feeding was assessed in non-deprived mice by measuring the intake of sweetened milk in a 30-minute period, as well as daily food pellet intake. LPS and mIL-1beta reliably reduced milk intake, and typically reduced food pellet intake. Treatment of the mice with peripherally administered alpha-adrenergic (phentolamine or prazosin) or beta-adrenergic (propranolol) antagonists, either alone or in combination, did not significantly alter the hypophagic responses to IL-1beta or LPS. Mice in which cerebral norepinephrine was depleted with DSP-4 or 6-hydroxydopamine also showed hypophagia in response to mIL-1b and LPS. The hypophagic responses to LPS and mIL-1beta were not affected by the dopamine receptor antagonist, haloperidol, the histaminergic antagonists, pyrilamine (H1) and cimetidine (H2), and an H3-antagonist, the muscarinic cholinergic antagonist, scopolamine. A variety of serotonin receptor antagonists, and 5,7-dihydroxytryptamine also failed to alter the responses. These results suggest that noradrenergic, dopaminergic, serotonergic, histaminergic and cholinergic systems are not essential for the hypophagia induced by LPS and IL-1, and that multiply redundant pathways may be involved in illness-related hypophagia.

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Presentation Number SAdunn0271
Keywords: Feeding Behavior, Interleukin-1, norepinephrine, serotonin