Toggle Main Menu Toggle Search

Open Access padlockePrints

The RNA of the glutamate transporter EAAT2 is variably spliced in amyotrophic lateral sclerosis and normal individuals

Lookup NU author(s): Dr Thomas Meyer, Dr Anne Fray, Professor Pamela Shaw

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


Abstract

Impaired re-uptake of synaptic glutamate, and a reduced expression of the glutamate transporter EAAT2 have been found in the motor cortex of patients with amyotrophic lateral sclerosis (ALS). Two splice forms of the EAAT2 RNA resulting from retention of intronic sequences (EAAT2/Int) and deletion of one protein coding exon (EAAT2/C1) have been reported to account for the EAAT2 protein loss in ALS. In this study we investigated the presence of two known (EAAT2/C1; EAAT2/Int) and three novel (EAAT2/C2-4) EAAT2 RNA in motor cortex of 17 ALS cases and 11 controls. Reverse transcription and PCR were carried out to amplify the complementary DNA of the complete and variably spliced EAAT2 transcripts. Nested PCR was followed to generate amplicons specific for EAAT2/C1-4 and EAAT2/Int. EAAT2/Int was detected in 59% of ALS specimens as compared to 36% of controls showing a trend but no statistical significance of a more frequent expression in ALS (Type I error 24.6%). EAAT2/C1-4 were found to be equally expressed in ALS patients and controls. Our results indicate that the involvement of EAAT2 transcripts in ALS is unlikely to be primary, and more complex than previously recognized. Alterations of quantitative expression of distinct EAAT2 splice forms in ALS cannot be excluded from this study and remain to be investigated.


Publication metadata

Author(s): Meyer T, Fromm A, Munch C, Schwalenstocker B, Fray AE, Ince PG, Stamm S, Gron G, Ludolph AC, Shaw PJ

Publication type: Article

Publication status: Published

Journal: Journal of the Neurological Sciences

Year: 1999

Volume: 170

Issue: 1

Pages: 45-50

Print publication date: 15/11/1999

ISSN (print): 0022-510X

ISSN (electronic): 1878-5883

Publisher: Elsevier

URL: http://dx.doi.org/10.1016/S0022-510X(99)00196-3

DOI: 10.1016/S0022-510X(99)00196-3

PubMed id: 10540035


Altmetrics

Altmetrics provided by Altmetric


Share