Polyinosinic:polycytidylic acid induces memory processing deficits in the day-old chick.

Anecdotal and experimental evidence has demonstrated that humans and animals exhibit physiological and cognitive alterations in response to sickness and injury. It is now clear that these changes are due to the actions of proinflammatory cytokines. The current study examined the effects of peripheral administration of polyinosinic:polycytidylic acid, a synthetic double-stranded viral RNA, on the memory processes of day-old chicks trained on a single trial passive avoidance task. Polyinosinic:polycytidylic acid impaired performance on the passive avoidance task in a dose-dependent manner. Maximal deficits were observed when 5 g/kg polyinosinic:polycytidylic acid was administered 120 min before training. Tests for retention revealed that interference in memory consolidation appeared between 30 and 40 min after training. These results indicate an inhibitory effect of polyinosinic:polycytidylic acid on the processes of memory formation at the transition from intermediate-term memory phase (A) to intermediate-term memory phase (B) of the Gibbs and Ng model of memory formation. The study also investigated the pyrogenic actions of polyinosinic:polycytidylic acid, and examined the effect of pretreatment with ketoprofen, a cyclooxygenase inhibitor. Significant rises in body temperature were observed 30 min after injection of polyinosinic:polycytidylic acid. Inhibition of cyclooxygenase by ketoprofen ameliorated the polyinosinic:polycytidylic acid-induced deficits in retention and attenuated the increase in body temperature. These results demonstrate that polyinosinic:polycytidylic acid induces memory processing deficits and is pyrogenic in the day-old chick and that these effects are cyclooxygenase-dependent.