Huntington Disease and Tourette Syndrome. II. Uptake of Glutamic Acid and Other Amino Acids by Fibroblasts

Overview

Journal Am J Hum Genet

Publisher Cell Press

Specialty Genetics

Date 1981 Mar 1

PMID 6452058

Citations 4

Authors

D E Comings

I E GOETZ

J Holden

J Holtz

Affiliations

Soon will be listed here.

Abstract

Injection of kainic acid, a rigid analog of the excitatory neurotransmitter glutamic acid (glu), into the neostriatum of rats produces a condition that mimics Huntington disease (HD) in at least 12 different morphological and biochemical parameters. These results suggested that one of the possible basic mechanisms in HD is a defect in the presynaptic of glial uptake of glu, resulting in chronic hyperstimulation and death of a specific set of neurons. To test this hypothesis, the uptake of glu was studied in 12 carefully matched sets of control-HD pairs and two lines of Tourette syndrome fibroblasts. Although the first six sets suggested a glutamate transport defect in HD cells, examination of 12 sets indicated that there were no significant differences between control and HD cells. The fibroblasts showed both a high and low affinity uptake of glutamic acid. Sodium dependent uptake of L-glutamate (L-glu) minus D-glutamate (D-glu) at 100, 1,000, and 10,000 Micrometers glutamate was normal in HD and Tourette syndrome cells.

Citing Articles

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