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      Role of Hypothalamic Histaminergic Neurons in Mediation of ACTH and Beta-Endorphin Responses to LPS Endotoxin in vivo

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          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 H<sub>3</sub> receptor agonist R(α)methylHA, which inhibits HA synthesis and release, decreased the response about 50%. Pretreatment with the H<sub>1</sub> receptor antagonist mepyramine (67 µg × 2 i.c.v.) inhibited the hormone response to LPS about 50%, while pretreatment with equimolar doses of the H<sub>1</sub> 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 H<sub>1</sub> 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 H<sub>2</sub> 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 H<sub>1</sub> receptors.

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          Author and article information

          S. Karger AG
          09 April 2008
          : 60
          : 3
          : 243-251
          aDepartment of Medical Physiology, Division of Endocrinology and Metabolism, The Panum Institute, and bDepartment of Surgical Gastroenterology, Hvidovre Hospital, University of Copenhagen, Denmark; cUnité de Neurobiologie et Pharmacologie, Unité 109, Institut National de la Santé et de la Recherche Médicale, Centre Paul Broca, Paris, France
          126757 Neuroendocrinology 1994;60:243–251
          © 1994 S. Karger AG, Basel

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          Page count
          Pages: 9
          Corticotropin Regulation and Corticoid Feedback


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