K Onodera, H Shinoda, M Imaizumi, E Hiraki-Sakurai, A Yamatodani
Index: Methods Find. Exp. Clin. Pharmacol. 16(8) , 575-81, (1994)
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The purpose of this study was to examine the effects of intracerebroventricular (i.c.v.) administration of N-acetylhistamine on rectal temperature, histamine level, histidine decarboxylase (HDC) activity, and the turnover rate of monoamines in mice. More than 60 micrograms of N-acetylhistamine induced hypothermia. The maximum effect of hypothermia was observed 20 min after administration of N-acetylhistamine (60-120 micrograms/mouse). A significant drop in rectal temperature of 3 degrees C was induced by 120 micrograms of N-acetylhistamine. Concurrent with the appearance of hypothermia, the histamine levels were increased. However, both histamine H1 and H2 antagonists did not prevent hypothermia. The i.c.v. administration of N-acetylhistamine inhibited HDC activity, but had no effect on the turnover rates of monoamines. These data confirmed that endogenous N-acetylhistamine may be a metabolite which lacks significant physiological roles, and demonstrated that exogenous N-acetylhistamine is not a good pharmacological tool for the study of the functions of the brain histaminergic system in mammals.
Structure | Name/CAS No. | Molecular Formula | Articles |
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N-ω-Acetylhistamine
CAS:673-49-4 |
C7H11N3O |
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