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Increase of extracellular brain calcium involved in interleukin‐1β‐induced pyresis in the rabbit: antagonism by dexamethasone
Author(s) -
Palmi M.,
Frosini M.,
Becherucci C.,
Sgaragli G.P.,
Parente L.
Publication year - 1994
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1994.tb13093.x
Subject(s) - extracellular , endocrinology , hyperthermia , medicine , calcium , egta , dexamethasone , chemistry , interleukin , prostaglandin e2 , calcium in biology , pharmacology , cytokine , biochemistry
1 This study investigates the role of extracellular brain calcium in the hyperthermia induced by interleukin‐1β (IL‐1β). 2 Intracerebroventricular (i.c.v.) injection of IL‐1β (12.5 ng kg −1 ) in rabbits caused a prompt and sustained rise in cerebrospinal fluid (CSF) Ca 2+ concentration ([Ca 2+ ]) followed by enhanced prostaglandin E 2 (PGE 2 ) release and hyperthermia. 3 A linear and significant correlation was observed between the increase in [Ca 2+ ] induced by IL‐1β and the rise in body temperature. 4 Ventriculo‐cisternal perfusion with artificial CSF containing the calcium chelator EGTA (1.3 m m ) 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 μg kg −1 ) 100 min prior to IL‐1β, dose‐dependently antagonized the cytokine‐induced Ca 2+ increase, the PGE 2 release and the febrile response. 6 These results suggest that changes in extracellular brain calcium are involved in the regulation of body temperature. In this light, the antipyretic action of Dex may be related to its effect on Ca 2+ uptake.