M. Palmi et al., INCREASE OF EXTRACELLULAR BRAIN CALCIUM INVOLVED IN INTERLEUKIN-1-BETA-INDUCED PYRESIS IN THE RABBIT - ANTAGONISM BY DEXAMETHASONE, British Journal of Pharmacology, 112(2), 1994, pp. 449-452
1 This study investigates the role of extracellular brain calcium in t
he hyperthermia induced by interleukin-1 beta (IL-1 beta). 2 Intracere
broventricular (i.c.v.) injection of IL-1 beta (12.5 ng kg(-1)) in rab
bits caused a prompt and sustained rise in cerebrospinal fluid (CSF) C
a2+ concentration ([Ca2+]) followed by enhanced prostaglandin E(2) (PG
E(2)) release and hyperthermia. 3 A linear and significant correlation
was observed between the increase in [Ca2+] induced by IL-1 beta and
the rise in body temperature. 4 Ventriculo-cisternal perfusion with ar
tificial CSF containing the calcium chelator EGTA (1.3 mM) blocked the
IL-1-induced PGE(2) release and countered the febrile response. 5 I.c
.v. administration of dexamethasone (Dex) (2.4 and 24 mu g kg(-1)) 100
min prior to IL-1 beta, dose-dependently antagonized the cytokine-ind
uced Ca2+ increase, the PGE(2) release and the febrile response. 6 The
se results suggest that changes in extracellular brain calcium are inv
olved in the regulation of body temperature. In this light, the antipy
retic action of Dex may be related to its effect on Ca2+ uptake.