The glial glutamate transporter in hyperammonemia and hepatic encephalopathy: Relation to energy metabolism and glutamatergic neurotransmission

Michael D. Norenberg, Zhifeng Huo, Joseph T. Neary, Ana Roig-Cantesano

Research output: Contribution to journalArticle

128 Scopus citations

Abstract

Abnormalities in glutamate metabolism and glutamatergic neurotransmission appear to play a major role in the pathogenesis of hyperammonemia and hepatic encephalopathy. Astrocytes may be involved in these derangements as ammonia has been shown to impair the ability of these cells to take up glutamate. This study presents a northern blot analysis of the GLT-1 glutamate transporter in hyperammonemic rats, and in rats with thioacetamide-induced acute liver failure. Our findings demonstrate a downregulation of GLT-1 mRNA in both conditions. This article examines the potential impact of deficits in glutamate uptake on energy metabolism and glutamatergic neurotransmission in the context of abnormalities in glial-neuronal interactions. We propose that an ammonia-induced abnormality in astroglial glutamate uptake constitutes a critical aspect in the pathogenesis of hepatic encephalopathy and other hyperammonemic conditions.

Original languageEnglish (US)
Pages (from-to)124-133
Number of pages10
JournalGlia
Volume21
Issue number1
DOIs
StatePublished - Sep 1 1997

Keywords

  • Ammonia
  • Ammonia neurotoxicity
  • Astrocytes
  • Cell swelling
  • Energy metabolism
  • Glial-neuronal interactions
  • GLT-1 glutamate transporter
  • Glutamate uptake

ASJC Scopus subject areas

  • Immunology

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