INCREASE OF EXTRACELLULAR BRAIN CALCIUM INVOLVED IN INTERLEUKIN-1-BETA-INDUCED PYRESIS IN THE RABBIT - ANTAGONISM BY DEXAMETHASONE

Citation
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
Citations number
20
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00071188
Volume
112
Issue
2
Year of publication
1994
Pages
449 - 452
Database
ISI
SICI code
0007-1188(1994)112:2<449:IOEBCI>2.0.ZU;2-4
Abstract
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.