Monoamine Oxidase Activity and Monoamine Metabolism in Brains of Parkinsonian Patients Treated with l ‐Deprenyl

Monoamine Oxidase Activity and Monoamine Metabolism in Brains of Parkinsonian Patients Treated... Abstract: Monoamine oxidase (MAO) type A and type B were measured using kynuramine, 3,4‐dihydroxyphenyl‐ethylamine (dopamine, DA), and 5‐hydroxytryptamine (5‐HT, serotonin) in 20 brain areas. The highest activities were found in the striatum (caudate nucleus, putamen, globus pallidus, and substantia nigra), hypothalamus, and c‐mammilare. The ratio of DA to 5‐HT deamination varied in the different regions, being in favor of DA in the striatum. With kynuramine as the substrate IC50 values of a number of inhibitors indicated that l‐deprenyl was far more potent an inhibitor of human brain MAO than clorgyline or harmaline. N‐Desmethylpropargylindane hydrochloride (AGN 1135) was also shown to have MAO‐B inhibitory selectivity similar to that of l‐deprenyl. Brains obtained at autopsy from l‐deprenyl‐treated Parkinsonian patients showed that, whereas MAO‐B was fully inhibited by the therapeutic doses of l‐deprenyl, substantial MAO‐A activity was still evident. These results are matched by the significant increases of DA noted in caudate nucleus, globus pallidus, putamen, and substantia nigra and the unaltered 5‐HT and 5‐hydroxyindoleacetic acid (5‐HIAA) in the same regions. These data indicate that the therapeutic actions of l‐deprenyl may lie in its selective inhibition of MAO‐B resulting in increased brain levels of DA formed from L‐dihydroxyphenylacetic acid (L‐DOPA). http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Neurochemistry Wiley

Monoamine Oxidase Activity and Monoamine Metabolism in Brains of Parkinsonian Patients Treated with l ‐Deprenyl

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Publisher
Wiley
Copyright
Copyright © 1986 Wiley Subscription Services, Inc., A Wiley Company
ISSN
0022-3042
eISSN
1471-4159
DOI
10.1111/j.1471-4159.1986.tb01747.x
Publisher site
See Article on Publisher Site

Abstract

Abstract: Monoamine oxidase (MAO) type A and type B were measured using kynuramine, 3,4‐dihydroxyphenyl‐ethylamine (dopamine, DA), and 5‐hydroxytryptamine (5‐HT, serotonin) in 20 brain areas. The highest activities were found in the striatum (caudate nucleus, putamen, globus pallidus, and substantia nigra), hypothalamus, and c‐mammilare. The ratio of DA to 5‐HT deamination varied in the different regions, being in favor of DA in the striatum. With kynuramine as the substrate IC50 values of a number of inhibitors indicated that l‐deprenyl was far more potent an inhibitor of human brain MAO than clorgyline or harmaline. N‐Desmethylpropargylindane hydrochloride (AGN 1135) was also shown to have MAO‐B inhibitory selectivity similar to that of l‐deprenyl. Brains obtained at autopsy from l‐deprenyl‐treated Parkinsonian patients showed that, whereas MAO‐B was fully inhibited by the therapeutic doses of l‐deprenyl, substantial MAO‐A activity was still evident. These results are matched by the significant increases of DA noted in caudate nucleus, globus pallidus, putamen, and substantia nigra and the unaltered 5‐HT and 5‐hydroxyindoleacetic acid (5‐HIAA) in the same regions. These data indicate that the therapeutic actions of l‐deprenyl may lie in its selective inhibition of MAO‐B resulting in increased brain levels of DA formed from L‐dihydroxyphenylacetic acid (L‐DOPA).

Journal

Journal of NeurochemistryWiley

Published: May 1, 1986

References

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