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Alterations in Glutamate Transporter Protein Levels in Kindling‐Induced Epilepsy
Author(s) -
Miller Heather Prince,
Levey Allan I.,
Rothstein Jeffrey D.,
Tzingounis Anastassios V.,
Conn P. Jeffrey
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68041564.x
Subject(s) - piriform cortex , kindling , amygdala , hippocampus , glutamate receptor , epilepsy , forebrain , neuroscience , limbic system , transporter , endocrinology , biology , medicine , cerebral cortex , central nervous system , chemistry , biochemistry , receptor , gene
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.