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B. Beasley, MD
Dept of Neurology US Public Health Service Hosp Staten Island, NY 10304

T. N. Chase, MD
National Institute of Neurological and Communicative Disorders and Stroke Bethesda, MD 20014

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.

In Reply.—

Dr Fuller misinterprets the basis for our conclusion. Our results with fenfluramine hydrochloride are consistent with findings obtained in other studies of drugs known to influence, by various mechanisms, serotonin-mediated synaptic function. Taken together, these clinical observations suggest that "serotonergic function plays no significant role in the pathogenesis of human parkinsonism."

We agree that the central pharmacologic actions of fenfluramine, like most drugs, are complex. The prevailing view, as stated in our article, is that fenfluramine acts primarily to augment serotonin system function by either inhibiting reuptake or stimulating postsynaptic serotonergic receptors. In either case, diminished serotonin synthesis presumably occurs as a secondary, compensatory phenomenon. A similar and much better studied situation occurs in the dopamine system, where dopamine agonists are well known to diminish transmitter synthesis in presynaptic dopaminergic neurons, while drugs that block postsynaptic dopamine receptors exert the opposite effect. Although at relatively high doses fenfluramine may block . . . [Full Text PDF of this Article]

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