Expression of glutamine transporter isoforms in cerebral cortex of rats with chronic hepatic encephalopathy

Renata Leke, Thayssa D.C. Escobar, Kakulavarapu V. Rama Rao, Themis Reverbel Silveira, Michael D. Norenberg, Arne Schousboe

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that occurs due to acute and chronic liver diseases, the hallmark of which is the increased levels of ammonia and subsequent alterations in glutamine synthesis, i.e. conditions associated with the pathophysiology of HE. Under physiological conditions, glutamine is fundamental for replenishment of the neurotransmitter pools of glutamate and GABA. The different isoforms of glutamine transporters play an important role in the transfer of this amino acid between astrocytes and neurons. A disturbance in the GABA biosynthetic pathways has been described in bile duct ligated (BDL) rats, a well characterized model of chronic HE. Considering that glutamine is important for GABA biosynthesis, altered glutamine transport and the subsequent glutamate/GABA-glutamine cycle efficacy might influence these pathways. Given this potential outcome, the aim of the present study was to investigate whether the expression of the glutamine transporters SAT1, SAT2, SN1 and SN2 would be affected in chronic HE. We verified that mRNA expression of the neuronal glutamine transporters SAT1 and SAT2 was found unaltered in the cerebral cortex of BDL rats. Similarly, no changes were found in the mRNA level for the astrocytic transporter SN1, whereas the gene expression of SN2 was increased by two-fold in animals with chronic HE. However, SN2 protein immuno-reactivity did not correspond with the increase in gene transcription since it remained unaltered. These data indicate that the expression of the glutamine transporter isoforms is unchanged during chronic HE, and thus likely not to participate in the pathological mechanisms related to the imbalance in the GABAergic neurotransmitter system observed in this neurologic condition.

Original languageEnglish (US)
Article number3688
Pages (from-to)32-37
Number of pages6
JournalNeurochemistry International
Volume88
DOIs
StatePublished - Sep 1 2015

Keywords

  • Chronic hepatic encephalopathy
  • GABA
  • Glutamine
  • Glutamine transporters

ASJC Scopus subject areas

  • Cellular and Molecular Neuroscience
  • Cell Biology

Fingerprint Dive into the research topics of 'Expression of glutamine transporter isoforms in cerebral cortex of rats with chronic hepatic encephalopathy'. Together they form a unique fingerprint.

  • Cite this