Alterations in glutamate transporter protein levels in kindling-induced epilepsy

Heather Prince Miller, Allan I. Levey, Jeffrey D. Rothstein, Anastassios V. Tzingounis, P. Jeffrey Conn

Research output: Contribution to journalArticle

Abstract

There is increasing evidence that levels of glutamate are elevated in certain brain regions immediately prior to and during induction and propagation of seizures. Modulation of high-affinity glutamate uptake is a potential mechanism responsible for the elevated levels observed with seizures. To date, three distinct Na+-dependent glutamate transporters have been cloned from rat and rabbit: GLT-1, GLAST, and EAAC-1. We performed a series of experiments to determine whether levels of these transporters are altered in amygdala-kindled rats. Levels of GLT-1, GLAST, and EAAC-1 were examined in three brain regions (hippocampus, piriform cortex/amygdala, and limbic forebrain) by quantitative immunoblotting using subtype-specific antibodies. GLAST protein was down-regulated in the piriform cortex/amygdala region of kindled rats as early as 24 h after one stage 3 seizure and persisting through multiple stage 5 seizures. In contrast, kindling induced an increase in EAAC-1 levels in piriform cortex/amygdala and hippocampus once the animals had reached the stage 5 level. No changes in GLT-1 were observed in any region examined. Changes in transporter levels could contribute to the changes in glutamate levels seen with kindling.

Original languageEnglish (US)
Pages (from-to)1564-1570
Number of pages7
JournalJournal of Neurochemistry
Volume68
Issue number4
DOIs
StatePublished - Apr 1997

Keywords

  • Epilepsy
  • Hippocampus
  • Piriform cortex
  • Seizure
  • Uptake

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

Fingerprint Dive into the research topics of 'Alterations in glutamate transporter protein levels in kindling-induced epilepsy'. Together they form a unique fingerprint.

  • Cite this