Abstract
The effect of nialamide on motility of mice kept in a familiar cage was investigated. Fifty and 100 mg/kg nialamide administered subcutaneously produced only weak hypermotility, while 200 mg/kg nialamide elicited strong and long-lasting hypermotility consisting of continuous jerky locomotion, head movements and tremor. The effect of 100 mg/kg nialamide was strongly potentiated by oral pretreatment with lithium chloride (250 mg/kg), chlorimipramine (20 and 50 mg/kg) and FG 4963 (20 and 50 mg/kg). Nialamide + FG 4963 produced a more prolonged hypermotility than chlorimipramine + nialamide. Pretreatment with the 5-hydroxytryptamine-synthesis inhibitor, p-chlorophenylalanine abolished potentiation of nialamide by lithium ion and reduced potentiation by chlorimipramine and FG 4963, indicating an involvement of 5-hydroxytryptamine. Nialamide (50 mg/kg s.c.) + l-tryptophan (50 mg/kg p.o.) induced moderate, short-lasting hypermotility, which was potentiated by chlorimipramine and FG 4963 but not by lithium ion, which suggests that lithium may act by increasing the concentration of l-tryptophan in brain.
Published Version
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