Wang H D, Wang Y P, Li C J, Lu D X, Yan L, Qi R B
Department of Pathophysiology, Medical College of Jinan University, Guangzhou, 510632.
Sheng Li Xue Bao. 1999 Apr;51(2):161-7.
The purpose of the present study was to investigate whether the antipyretic effect of dexamethasone (DEX) delivered by intravenous injection (i.v.) on intracerebroventricularly (icv) administered egtazic acid-induced febrile response is relevant to the changes in cytosolic free calcium concentration of the hypothalamus. The colon temperatures were measured by a thermistor and the cytosolic free calcium concentration ([Ca2+]i) in dissociated brain cells was measured by Fura 2-AM. The results demonstrated that the pyretic action of egtazic acid (0.6 mumol, icv) was markedly inhibited by DEX (5 mg/kg, i.v.), but DEX (60-120 mumol/L) did't affect [Ca2+]i in dissociated hypothalamus cells. Actinomycin D, which interferes with gene transcription (3 nmol, icv), completely abolished the antipyretic action of DEX on egtazic acid-induced fever. These findings suggest that the antipyretic action of DEX on egtazic acid-induced fever is related to the activation of certain gene expression in the brain, but not to the changes of transmembrane calcium ion current in hypothalamus neurons.
