Glutamate transporter gene expression in amyotrophic lateral sclerosis motor cortex

Lynn A. Bristol, Jeffrey D Rothstein

Research output: Contribution to journalArticle

Abstract

Glutamate transport is critical for synaptic inactivation of glutamate and prevention of excitotoxicity. The following four glutamate transporters have been identified in human brain: EAAT1, EAAT2, EAAT3, and EAAT4. Deficient glutamate transport has been identified in the motor cortex and the spinal cord of tissue from amyotrophic lateral sclerosis (ALS) patients. The defect appears to be due to a selective loss of the astroglial specific glutamate transporter protein EAAT2. In these studies we sought to extend our understanding of glutamate transporters in ALS by examining the mRNA for each transporter subtype in ALS motor cortex. All tissue was matched for age and postmortem delay. There was no quantitative change in mRNA for EAAT1, EAAT2, or EAAT3 in ALS motor cortex, even in patients with a large loss of EAAT2 protein (95% decrease compared with control) and decreased tissue glutamate transport (73% decrease compared with control). These studies suggest that the dramatic abnormalities in EAAT2 may be due to translational or posttranslational processes.

Original languageEnglish (US)
Pages (from-to)676-679
Number of pages4
JournalAnnals of Neurology
Volume39
Issue number5
DOIs
StatePublished - May 1996

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Amino Acid Transport System X-AG
Amyotrophic Lateral Sclerosis
Motor Cortex
Glutamic Acid
Gene Expression
Messenger RNA
Spinal Cord
Proteins
Brain

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Glutamate transporter gene expression in amyotrophic lateral sclerosis motor cortex. / Bristol, Lynn A.; Rothstein, Jeffrey D.

In: Annals of Neurology, Vol. 39, No. 5, 05.1996, p. 676-679.

Research output: Contribution to journalArticle

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