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Neuroendocrine function in Huntington's disease: dopaminergic regulation of prolactin release.
Authors:E Caine  R Kartzinel  M Ebert  A C Carter
Institution:1. Section on Experimental Therapeutics, Laboratory of Clinical Science National Institute of Mental Health, Bethesda, Maryland 20014, USA;2. The State University of New York, Downstate Medical Center, Brooklyn, New York, USA
Abstract:Plasma prolactin levels were measured in 7 patients with Huntington's disease (HD) and 8 age matched controls after the random, oral administration of 1) placebo, 2) chlorpromazine 100 mg, 3) carbidopa 50 mg followed by levodopa 200 mg, and 4) bromocriptine 1 mg. After placebo, HD patients had significantly higher prolactin levels than controls at all times except 180, 240, and 360 minutes. Controls showed a significant suppression of prolactin release at 180 and 240 minutes after levodopa/carbidopa and at 180, 240, and 360 minutes after bromocriptine. In contrast, HD patients demonstrated no change after both levodopa/carbidopa and bromocriptine. Both groups showed a sustained elevation after CPZ, but despite having an initially higher baseline and an earlier response, the maximum prolactin levels of HD patients were significantly less than those of controls.This data suggest that HD patients may have a diminished number of hypothalamic-pituitary dopamine receptors for the regulation PRL secretion.
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