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Effect of Serotonin Depletion

Thomas N. Chase, MD; August M. Watanabe, MD; H. Keith H. Brodie, MD; Edward F. Donnelly, PhD

Arch Neurol. 1972;26(3):282-284.

Abstract
Fenclonine (DL-parachlorophenylalanine), a potent inhibitor of serotonin synthesis, was administered to six patients with Huntington's chorea. Doses sufficient to reduce the cerebrospinal fluid (CSF) content of 5-hydroxyindoleacetic acid (5-HIAA), the principal catabolite of serotonin by nearly 50%, produced no consistent alteration in motor or behavioral function. The pretreatment concentration of 5-HIAA in CSF was in the normal range. Cerebrospinal fluid levels of homovanillic acid, a major catabolite of dopamine, did not change during drug treatment. The results thus fail to support the hypothesis that hyperfunction of serotonin-containing neural systems plays a crucial role in the pathogenesis of Huntington's disease.

Author Affiliations
Bethesda, Md

From the Neurology Unit, National Institute of Mental Health, Bethesda, Md.

Footnotes
Accepted for publication Nov 8, 1971.

Reprint requests to Neurology Unit, National Institute of Mental Health, Bethesda, Md 20014 (Dr. Chase).

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