Abstract
Harmaline (30 mg/kg), injected intraperitoneally into rats, causes a decrease in body temperature. Treatment with either α-methyl-dopa (200 mg/kg, i.p.) or with a-methyltyrosine (200 mg/kg, i.p.) 24 hr before, or with p-chlorophenylalanine (315 mg/kg, i.p.) 72 hr before injection of haarmaline, did not influence the decrease in temperature. Reserpine (5 mg/kg, i.p.) given 24 hr before harmaline did not affect the temperature fall caused by the latter drug. However, administration of Ro-4-4602 (693 mg/kg, i.p.), an inhibitor of dopa decarboxylase, or sodium diethyldithiocarbamate (360 mg/kg, i.p.) 24 hr after reserpine and 1 hr before the injection of harmaline prevented the fall in temperature ( p <0.05). Administration of harman (25 mg/kg), and harmalol (28 mg/kg), two derivatives of harmaline, also caused a fail in body temperature. The compounds harmaline, harman and harmalol, all antagonized the action of serotonin on the rat uterus. Distribution between free and bound serotonin and free and bound noradrenaline in rat brain (omitting the cerebellum), 1or 2 hr after the administration of harmaline, did not differ significantly from that observed in brains of saline-teeated controls. The results suggest that the decrease in body temperature after the administration of harmaline may be the consequence of a disturbance of monoamine relationship at brain thermoreceptor sites.
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