Chlorimipramine, fenfluramine and quipazine decrease 5-hydroxytryptamine synthesis in discrete rat brain nuclei.

Abstract:

:A procedure for studying 5-hydroxytryptamine synthesis by determining the rate of accumulation of 5-hydroxytryptophan after administering m-hydroxybenzylhydrazine, an inhibitor of aromatic-l-amino acid decarboxylase, and large doses of l-tryptophan was characterized. The utility of this method as an index of 5-hydroxytryptamine neuronal activity was studied by determining the effects on 5-hydroxytryptophan accumulation of direct and indirect 5-hydroxytryptamine agonists; viz, chlorimipramine-a 5-hydroxytryptamine uptake inhibitor, fenfluramine-a 5-hydroxytryptamine releaser, and quipazine-a 5-hydroxytryptamine receptor agonist. In the absence of m-hydroxybenzylhydrazine pretreatment 5-hydroxytryptophan and the dopamine precursor 3,4-dihydroxyphenylalanine were not readily detectable in any brain region studied. They both accumulated after m-hydroxybenzylhydrazine treatment in a time-dependent manner with the 30 min time point being on the linear portion of the curve. Administration of l-tryptophan 60 min before sacrifice increased 5-hydroxytryptophan, but not 3,4-dihydroxyphenylalanine, in a dose-related manner with the peak effect occurring after 100-300 mg/kg. Chlorimipramine, fenfluramine and quipazine all decreased 5-hydroxytryptophan, but not 3,4-dihydroxyphenylalanine, in m-hydroxybenzylhydrazine and l-tryptophan-treated animals. Chlorimipramine produced these effects in a dose-related manner only after l-tryptophan loading and without affecting brain concentrations of l-tryptophan. These results suggest that the measurement of 5-hydroxytryptophan after l-tryptophan administration and aromatic-l-amino acid decarboxylase inhibition might serve as a useful index of 5-hydroxytryptamine synthesis.

journal_name

Neurochem Int

authors

Nielsen JA

doi

10.1016/0197-0186(86)90014-8

subject

Has Abstract

pub_date

1986-01-01 00:00:00

pages

403-12

issue

3

eissn

0197-0186

issn

1872-9754

pii

0197-0186(86)90014-8

journal_volume

8

pub_type

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