Open AccessHypothalamic Neuronal Histamine Modulates Adaptive Behavior and Thermogenesis in Response to Endogenous Pyrogen
Author(s) -
Sakata Toshiie,
Rang Masahiro,
Kurokawa Mamoru,
Yoshimatsu Hironobu
Publication year - 1995
Publication title -
obesity research
Language(s) - English
Resource type - Journals
eISSN - 1550-8528
pISSN - 1071-7323
DOI - 10.1002/j.1550-8528.1995.tb00489.x
Subject(s) - histamine , thermogenesis , endocrinology , medicine , histidine decarboxylase , prostaglandin e2 , hypothalamus , chemistry , endogeny , histaminergic , thermoregulation , biology , enzyme , adipose tissue , biochemistry , histidine
Homeostatic involvement of hypothalamic neuronal histamine in adaptive behavior and thermogenesis was investigated when interleukin‐1β (IL‐1β), one of the endogenous pyrogens, was infused peripherally in rats. IL‐1β decreased food and water intake and elevated body temperature. Depletion of neuronal histamine in the hypothalamus induced by α‐fluoromethylhistidine, a suicide inhibitor of the histamine synthesizing enzyme histidine decarboxylase (HDC), attenuated the suppressive effect of IL‐1β on food intake, facilitated the inhibitory effect on water intake, and enhanced its thermogenic effect. Simultaneously IL‐1β increased activity of HDC and histamine‐N‐methyltransferase (HMT), a neuronal histamine catabolizing enzyme. Pretreatment with indomethacin completely blocked those increases in turnover of neuronal histamine induced by IL‐1β. Hypothalamic prostaglandin E 2 (PGE 2 ) activated by peripheral IL‐1β, but not peripheral PGE 2 , increased both activities of HDC and HMT. Ginsenoside Rg 1 a major component of panax ginseng, modulated the suppressive effects of IL‐1β on ingestive behavior, resulting in a lowering of body temperature. The findings suggest that the effects of IL‐1β on ingestive behavior and thermogenesis may be modulated by dynamics of hypothalamic neuronal histamine through activation of hypothalamic PGE 2 which is elevated by peripheral IL‐1β.