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R. W. Fuller, PhD
The Lilly Research Laboratories Eli Lilly & Co Indianapolis, IN 46206

Arch Neurol. 1977;34(11):720.

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

To the Editor.—

Beasley et al (Arch Neurol 34:255, 1977) reported that fenfluramine hydrochloride did not alter extrapyramidal signs in parkinsonian patients and concluded that "serotonin-active drugs afford no significant therapeutic benefit to patients with this disorder." They gave fenfluramine on the assumption that it would enhance serotoninergic neurotransmission by inhibiting the reuptake of serotonin or by directly stimulating postsynaptic serotonin receptors. I contend that the action of fenfluramine is too complex to permit the conclusion they reached.

In contrast to agents that act simply to inhibit serotonin reuptake (fluoxetine, chlorimipramine) or to a serotonin-receptor stimulant (quipazine), which cause no change or a slight increase in serotonin concentration,^1,2 fenfluramine markedly decreases serotonin concentration in rat brain.^3,4 This decrease probably results mainly from inhibition of serotonin synthesis. Fenfluramine resembles P-chloroamphetamine in causing a long-lasting decrease in tryptophan hydroxylase,³ the rate-limiting enzyme in serotonin . . . [Full Text PDF of this Article]

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