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R. Tissot, MD; G. Bartholini, MD; A. Pletscher, MD, PhD

Arch Neurol. 1969;20(2):187-190.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

IN ANIMALS, Ro 4-4602 (N¹-[DL-seryl]-N²-[2,3,4-trihydroxybenzyl] -hydrazine) in doses of 5-50 mg/kg has been shown to cause a selective inhibition of decarboxylase of aromatic amino acids in extracerebral tissues. As a consequence, the drug markedly enhances the increase of dopa (3,4-dihydroxyphenylalanine) and methyldopa which occurs in the blood after intravenous and oral administration of dopa. The catecholamines and their metabolites (mainly phenolcarboxylic acids [PCA]) are, however, decreased as compared to animals treated with dopa alone. In the brain, especially in the extrapyramidal centers, the dopa-induced rise of dopamine is markedly enhanced by Ro 4-4602. This effect has been explained by an increased supply of dopa from the blood to the brain where formation of dopamine takes place since cerebral decarboxylase is not inhibited.^1-3

An increase of dopamine in extrapyramidal brain centers without a major rise of catecholamines in the extracerebral organs might be of interest . . . [Full Text PDF of this Article]

Author Affiliations
Geneva; Basle, Switzerland

From the University of Geneva (Dr. Tissot) and F. Hoffman-La Roche & Co., Ltd., Basle, Switzerland (Drs. Bartholini and Pletscher).

Footnotes
Submitted for publication, April 5, 1968; accepted May 7.

Reprint requests to F. Hoffman-La Roche & Co., Ltd., 4002 Basle, Switzerland (Prof A. Pletscher).

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