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 journalArticlepeer-review


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
Issue number4
StatePublished - Apr 1997


  • Epilepsy
  • Hippocampus
  • Piriform cortex
  • Seizure
  • Uptake

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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