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Effect of Endotoxin and Interleukin‐1β on Corticotropin‐Releasing‐Factor and Prostaglandin Release by Rat Brainstem Slices
Author(s) -
Francisco Molina-Holgado,
José Borrell,
Carmen Guaza
Publication year - 1998
Publication title -
journal of neuroendocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.062
H-Index - 116
eISSN - 1365-2826
pISSN - 0953-8194
DOI - 10.1046/j.1365-2826.1998.00222.x
Subject(s) - medicine , endocrinology , prostaglandin e2 , brainstem , stimulation , prostaglandin e , lipopolysaccharide , in vivo , ex vivo , prostaglandin , cytokine , chemistry , interleukin , biology , microbiology and biotechnology
This study investigated the effects of lipopolysaccharide (LPS) and interleukin‐1 β (IL‐1 β ) on corticotropin releasing factor (CRF) and prostaglandin E 2 (PGE 2 ) release by brainstem slices in vitro . First, we characterized our experimental model and demonstrated that high potassium stimulates CRF release from rat brainstem slices in a calcium dependent way. The direct stimulation of brainstem slices with IL‐1 β (3–25 pM) did not modify basal or potassium‐stimulated CRF release, although IL‐1 β at the dose of 25 pM increased PGE 2 production. Peripheral injection (ip) of LPS (1–10 μg/kg) or IL‐1 β (1–10 μg/kg) evoked a dose‐related potentiation of the ex‐vivo release of CRF and PGE 2 from brainstem slices. However, central (icv) administration of LPS (10–500 ng/rat) potentiated the release of CRF and PGE 2 only at the dose of 500 ng/rat, whereas IL‐1 β (1–100 ng/rat) failed to modify significantly the ex vivo production of both CRF and PGE 2 . The results of the present study provide evidence that peripheral, rather than central, endotoxin and IL‐1 β administration induce the activation of brainstem CRF and PGE 2 , supporting the hypothesis that peripheral cytokine signalling to the CNS is mediated by stimulation of peripheral afferents.