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What excitotoxin kills striatal neurons in Huntington's disease? Clues from neurochemical studies

Department of Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, Canada.

Amino acid analyses of both caudate nucleus and putamen obtained at autopsy from patients dying with Huntington's disease (HD), and from control subjects, showed significantly decreased mean glutamate contents in the HD patients. In addition, the mean glutamate concentration was significantly increased in the CSF of living HD patients as compared with controls. Neurochemical studies also showed that neither aspartic acid, proline, 5-oxoproline, nor homocysteic acid is likely to act as a causative excitotoxin in HD. Excessive striatal glycine content, or deficient glutathione content, is unlikely to contribute to the effects of a causative excitotoxin in HD. We suggest that glutamic acid may be the proximate causative neurotoxin in the striatum in HD, as a result of an unexplained failure in the reuptake mechanism for glutamate released there as an excitatory neurotransmitter.

Address correspondence and reprint requests to Dr. Thomas L. Perry, Department of Pharmacology and Therapeutics, University of British Columbia, Vancouver BC V6T 1W5, Canada.

Supported by the Medical Research Council of Canada.

Received March 13, 1989. Accepted for publication in final form June 14, 1989.

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