Aging is associated with a blunted or absent fever response to naturally oc
curring infections or to the peripheral administration of bacterial product
s 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 investiga
ted the fever response of young (3-5-month) and old (24-26-month) Long-Evan
s rats to the intracerebroventricular (i.c.v.) microinfusion of prostagland
in 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 r
ats. i.c.v. administered PGE(2) (100ng) induced comparable increases in bod
y temperature in young and old Long-Evans rats. In the two groups, PGE(2)-i
nduced fever was similar both in latency-to-peak fever and maximal fever re
sponse. These data, and the previous data on IL-1 beta, demonstrate that th
e 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 immunomodulator
s. (C) 1999 Elsevier Science Inc.