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National Institute of Neurologic and Communicative Disorders and Stroke, Experimental Therapeutics Branch, Bethesda, MD, and The Maryland Psychiatric Research Center, Department of Psychiatry, University of Maryland, Baltimore, MD.
We studied the acute effects of pharmacologic stimulation of neurotransmitter systems implicated in growth hormone and prolactin regulation in eight patients with Huntington's disease and matched control subjects. Both apomorphine, a dopamine agonist, and muscimol, a GABA agonist, produced an exaggerated rise in plasma growth hormone levels in the Huntington patients. Neither the growth hormone response to a muscarinic agonist, arecoline, nor the prolactin response to any of these drugs differed in the patients and controls. Loss of somatostatin activity in the hypothalamic-pituitary axis in Huntington's disease could account for these endocrinologic changes.
Address correspondence and reprint requests to Dr. Tamminga, Maryland Psychiatric Research Center, University of Maryland, PO Box 3235, Baltimore, MD 21228.
Presented in part at the thirty-fourth Annual Meeting of the American Academy of Neurology, Washington, DC, April 1982.
Accepted for publication January 26, 1983.
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