Performance more than working memory disrupted by acute systemic inflammation in rats in appetitive tasks.

Evidence from molecular biology, epidemiology, behavioral pharmacology, and clinical science support the conclusion that brain inflammation contributes to the pathogenesis of cognitive symptoms in Alzheimer's disease (AD) and other neuropsychological disorders. Three different tests were conducted to determine whether the acute inflammatory response induced by systemic lipopolysaccharide (LPS) treatment is accompanied by a selective disruption of working memory functioning in rats. Doses of LPS sufficient to induce a thermoregulatory response were administered intraperitoneally and their effects on behavioral measures of symbolic working memory, spatial learning, and spatial memory consolidation, were assessed. LPS-induced immune activation was found not to significantly affect memory processes in any of the behavioral tests used. However, LPS-induced immune activation caused performance deficits consistent with a disruptive effect of LPS on motivation and arousal. These results suggest that sickness behavior induced by immune stimulation is not necessarily accompanied by selective impairment in memory processes. The importance of distinguishing cognitive disruption from performance impairment in interpreting the behavioral effects of inflammatory mediators is discussed.