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NEUROLOGY 1984;34:663
© 1984 American Academy of Neurology

Somatostatin is increased in the nucleus accumbens in Huntington's disease

M. Flint Beal, MD, Edward D. Bird, MD, Philip J. Langlais, MA and Joseph B. Martin, MD, PhD

From the Department of Neurology, Massachusetts General Hospital and McLean Hospital, and Harvard Medical School, Boston, MA 02114.

Concentrations of somatostatin-like immunoreactivity (SLI) are elevated in the basal ganglia in Huntington's disease. The present study confirms these findings and, in addition, shows that concentrations of SLI are significantly elevated in the nucleus accumbens (4.04 ± 0.66 versus 1.69 ± 0.21 ng/mg protein in controls). This area is relatively spared pathologically and shows little atrophy in Huntington's disease. Since many patients with Huntington's disease are treated with haloperidol, we studied the effects of this drug in rats. There was a dose-dependent reduction of SLI in striatum, parietal cortex, and hippocampus. The elevated concentrations of SLI in the basal ganglia in Huntington's disease, therefore, do not appear to result from haloperidol therapy.

Address correspondence and reprint requests to Dr. Beal, Neurology Research 4, Massachusetts General Hospital, Boston, MA 02114.

Supported by Huntington's Disease Center without Walls (National Institutes of Health grant NS 16367), and National Institutes of Health grant RO1-MHINS 31862 (EDB), RO1-AM-26252 (JBM) and the Julieanne Dorn Fund. Dr. Beal is a fellow of the National Huntington's Disease Association.

Accepted for publication September 9, 1983.




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J. B. Gramsbergen, L. Veenma-Van der Duin, K. Venema, and J. Korf
Cerebral Cation Shifts and Amino Acids in Huntington's Disease
Arch Neurol, December 1, 1986; 43(12): 1276 - 1281.
[Abstract] [PDF]




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