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The present study used a taste aversion paradigm to condition lipopolysaccharide (LPS)-induced suppression of splenic lymphocyte interleukin-2 (IL-2) production, with concurrent measurement of corticosterone production and splenic norepinephrine (NE) content). In training, two groups of rats received saccharin and IP LPS in a paired (P) manner and a third group in a specifically unpaired (U) manner. In the test, the unpaired group (group U) and one of the paired (group P) groups were re-exposed (R) to the cue and the other not (NR). An additional group controlled for the effects of cues (conditional stimulus) and fluid deprivation (negative control; NC). A robust taste aversion in the P-R group was accompanied by suppression of IL-2 production, reduced splenic NE content, and elevated corticosterone production, relative to combined controls (i.e., groups U-R, P-NR, and NC). The conditioned modulation of IL-2 secretion, along with the concomitant alteration of adrenocortical and sympathetic mediators, supports the involvement of bidirectional central nervous-immune system pathways in this paradigm.

In a previous investigation with mice, the paired presentation of either odor or taste cues with the peripheral (IP) administration of the immunoactive peptide interleukin-1 (IL-1) led to the conditioned enhancement of glucocorticoid production. The present study found that an initial central infusion of IL-1 in the presence of saccharin cues produced a robust taste aversion but not a conditioned elevation of either ACTH or corticosterone production. These results indicate that the glucocorticoid response induced by centrally administered IL-1 in rats is independent of the behaviorally aversive properties of this cytokine which are conditionable. The differential effects of IP versus ICV administration of IL-1 on glucocorticoid conditioning requires a clearer specification of the respective signaling mechanisms and pathways activated by these two routes of administration.