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L. Frattola, MD; M. G. Albizzatir, MD
Dept of Neurology

M. Trabucchi, MD
Dept of Pharmacology University of Milan Medical School, Milan, Italy

Arch Neurol. 1978;35(1):60.

	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.—

In a recent article in the ARCHIVES (33:517, 1976) and in a reply to a letter from Drs Tolosa and Sparber (34:58, 1977), Kartzinel and Calne reported that they "could not find any evidence to support the view that the dopaminergic agonist that we were studying, bromocriptine, had any therapeutic action in Huntington's disease." As we recently published,¹ bromocriptine exerts a mixed agonist-antagonist activity on the dopaminergic receptors, which are not competitively blocked by the drug. Moreover since bromocriptine reduces 3,4-dihydroxyphenylacetic acid (DOPAC) levels in the striatum,² a fact which may suggest a decrease of dopamine turnover in this area, one could expect a further decreased dopaminergic stimulation on the postsynaptic receptors.

On the other hand, bromocriptine at higher dosage stimulates the postsynaptic dopaminergic receptors, increasing the formation of cyclic adenosine monophosphate in vivo¹ by a mechanism that requires an intact dopamine-storage system. . . . [Full Text PDF of this Article]

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