Tardive decrease of astrocytic glutamate transporter protein in transgenic mice with ALS-linked mutant SOD1

H. Warita, Y. Manabe, T. Murakami, M. Shiote, Y. Shiro, T. Hayashi, I. Nagano, M. Shoji, K. Abe

Research output: Contribution to journalArticle

20 Citations (Scopus)

Abstract

The expressions of glutamate transporter proteins were immunocytochemically examined in the spinal cord of transgenic mice harboring a Gly93 → Ala (G93A) mutant human SOD1 gene. Astroglial EAAT2 protein level was preserved in the ventral horn even after the beginning of paralysis, and finally decreased at terminal stage of the disease (35 weeks of age), when neuronal EAAT3 protein level was also decreased. In contrast, glial fibrillary acidic protein (GFAP) immunoreactivity progressively increased from 25 weeks of age in the ventral horn. The present results show interesting dissociative expressions of astroglial proteins EAAT2 and GFAP in the same ventral horn, but suggest not an early and primary role of EAAT2 in the motoneuronal death of this model.

Original languageEnglish
Pages (from-to)577-581
Number of pages5
JournalNeurological Research
Volume24
Issue number6
DOIs
Publication statusPublished - Sep 1 2002
Externally publishedYes

Keywords

  • ALS
  • EAAT
  • Glutamate
  • Glutamate transporter
  • SOD1
  • Transgenic mouse

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Fingerprint Dive into the research topics of 'Tardive decrease of astrocytic glutamate transporter protein in transgenic mice with ALS-linked mutant SOD1'. Together they form a unique fingerprint.

  • Cite this

    Warita, H., Manabe, Y., Murakami, T., Shiote, M., Shiro, Y., Hayashi, T., Nagano, I., Shoji, M., & Abe, K. (2002). Tardive decrease of astrocytic glutamate transporter protein in transgenic mice with ALS-linked mutant SOD1. Neurological Research, 24(6), 577-581. https://doi.org/10.1179/016164102101200384