Role of Hypothalamic Histaminergic Neurons in Mediation of ACTH and Beta-Endorphin Responses to LPS Endotoxin in vivo
作者:
Ulrich Knigge,
Andreas Kjær,
Henrik Jørgensen,
Monique Garbarg,
Christian Ross,
Agnes Rouleau,
Jørgen Warberg,
期刊:
Neuroendocrinology
(Karger Available online 1994)
卷期:
Volume 60,
issue 3
页码: 243-251
ISSN:0028-3835
年代: 1994
DOI:10.1159/000126757
出版商: S. Karger AG
关键词: Histamine;Histamine receptors;β-Endorphin;Cytokines;Stress;Neuroimmune interactions;Corticotropin;Endotoxins
数据来源: Karger
摘要:
The involvement of hypothalamic histaminergic neurons in the mediation of the ACTH and β-endorphin (β-END) response to lipopolysaccharide (LPS) endotoxin was investigated in conscious male rats. LPS stimulated the release of ACTH and β-END dose-dependently and increased the hypothalamic concentration of the histamine (HA) metabolite tele-methylhistamine significantly and that of HA slightly, indicating an increased turnover of neuronal HA. Pretreatment with the HA synthesis inhibitor α-fluoromethyl-histidine administered intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) inhibited the ACTH and β-END response to LPS about 60%, whereas i.p. administration of the H3 receptor agonist R(α)methylHA, which inhibits HA synthesis and release, decreased the response about 50%. Pretreatment with the H1 receptor antagonist mepyramine (67 µg × 2 i.c.v.) inhibited the hormone response to LPS about 50%, while pretreatment with equimolar doses of the H1 receptor antagonists cimetidine (67 µg × 2 i.c.v.) or ranitidine (83 µg × 2 i.c.v.) had no effect on the LPS-induced release of ACTH and β-END. When the H1 receptor antagonists mepyramine and cetirizine were administered i.p. in doses (10 mg/kg) which penetrate the blood-brain barrier the hormone response to LPS was inhibited 50% and 30%, respectively. Administered i.p. the H2 receptor antagonists had no effect on the hormone response to LPS. We conclude that hypothalamic histaminergic neurons in rats are involved in the mediation of the ACTH and β-END response to LPS stimulation via activation of central postsynaptic H1
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