Prostaglandin E2-induced fever in young and old Long-Evans rats

Aging is associated with a blunted or absent fever response to naturally occurring infections or to the peripheral administration of bacterial products and proinflammatory cytokines. We have recently shown that old Long-Evans rats are not defective in their capacity to develop a fever in response to brain administration of interleukin-1 beta (IL-1 beta). Here, we investigated the fever response of young (3-5-month) and old (24-26-month) Long-Evans rats to the intracerebroventricular (i.c.v.) microinfusion of prostaglandin E-2 (PGE(2)), a final common mediator for the production of fever in the brain. Core body temperature was monitored by telemetry in freely moving rats. i.c.v. administered PGE(2) (100ng) induced comparable increases in body temperature in young and old Long-Evans rats. In the two groups, PGE(2)-induced fever was similar both in latency-to-peak fever and maximal fever response. These data, and the previous data on IL-1 beta, demonstrate that the brains of old and young rats are similar with respect to fever generation in response to the i.c.v. administration of two classes of immunomodulators. (C) 1999 Elsevier Science Inc.