Changes in mouse brain serotonin turnover following chronic imipramine administration.
Mice were injected daily for 2 weeks with saline, tryptophan or p-chlorophenylalanine, alone or in combination with the tricyclic antidepressant imipramine. Serotonin turnover in several brain regions was determined by the accumulation of serotonin after pargyline and 5-hydroxyindoleacetic acid after probenecid. Both methods agreed closely. Imipramine tended to depress serotonin turnover. This effect was more marked in hypothalamus, which has high serotonin activity, and was much less in cerebellum, which has low serotonin activity. Chronic imipramine treatment completely abolished the increase in serotonin turnover induced by tryptophan, but had no effect on serotonin turnover in mice treated with p-chlorophenylalanine, which itself reduced serotonin activity.
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D000818:Animals; D001923:Brain Chemistry / Q000187:drug effects*; D005260:Female; D010134:Fenclonine / Q000494:pharmacology; D006897:Hydroxyindoleacetic Acid / Q000378:metabolism; D007031:Hypothalamus / Q000378:metabolism; D007099:Imipramine / Q000008:administration & dosage / Q000494:pharmacology*; D007274:Injections, Intraperitoneal; D051379:Mice; D008995:Monoamine Oxidase / Q000378:metabolism; D010293:Pargyline / Q000494:pharmacology; D012701:Serotonin / Q000378:metabolism*; D013997:Time Factors; D014364:Tryptophan / Q000378:metabolism / Q000494:pharmacology
D012701:Serotonin; D006897:Hydroxyindoleacetic Acid; D014364:Tryptophan; D010293:Pargyline; D008995:Monoamine Oxidase; D007099:Imipramine; D010134:Fenclonine