Role of excitatory amino acid transporter 1 in neonatal rat neuronal damage induced by hypoxia-ischemia

F. Tao, S. D. Lu, L. M. Zhang, Y. L. Huang, F. Y. Sun

Research output: Contribution to journalArticle

Abstract

The role of excitatory amino acid transporter 1 in neonatal rat neuronal damage was studied following hypoxia-ischemia. To induce hypoxia-ischemia injury, rats on postnatal day 7 were exposed to 8% oxygen for 2 h following unilateral common carotid artery ligation. According to brain damage scoring based on Cresyl Violet staining, the neuronal damage time-dependently changed in the ischemic regions following hypoxia-ischemia. Immunohistochemical studies showed that excitatory amino acid transporter 1 expression was mainly observed in the cerebral cortex ipsilateral to common carotid artery ligation and markedly increased at 24 h and 48 h following hypoxia-ischemia. Combined with confocal laser scanning microscopic analysis, double staining showed that excitatory amino acid transporter 1 positive staining appeared in neurons as well as astrocytes after hypoxia-ischemia. Most excitatory amino acid transporter 1 positive staining cells exhibited regular morphological characteristics and only a few were double-stained by terminal deoxynucleotidyl transferase-mediated deoxyuridinetriphosphate nick-end labeling. Down-regulation of excitatory amino acid transporter 1 expression by intraventricular administration of specific antisense oligonucleotide exacerbated neuronal damage in hypoxia-ischemia brain. These results suggest that the increase of excitatory amino acid transporter 1 expression may be involved in a pathophysiological process of hypoxia-ischemia brain damage and may reflect a self-compensative mechanism for protecting neurons from further injury.

Original languageEnglish (US)
Pages (from-to)503-513
Number of pages11
JournalNeuroscience
Volume102
Issue number3
DOIs
StatePublished - Feb 5 2001

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Keywords

  • Anoxia
  • Antisense
  • Brain injuries
  • Double staining
  • Ischemia
  • Protection

ASJC Scopus subject areas

  • Neuroscience(all)

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