Alterations in glutamate transporter protein levels in kindling-induced epilepsy.

Miller HP, Levey AI, Rothstein JD, Tzingounis AV, Conn PJ
J Neurochem. 1997 68 (4): 1564-70

PMID: 9084427 · DOI:10.1046/j.1471-4159.1997.68041564.x

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.

MeSH Terms (16)

Amino Acid Transport System X-AG Animals ATP-Binding Cassette Transporters Biological Transport Blotting, Western Brain Chemistry Cerebral Cortex Epilepsy Glucose Transporter Type 1 Hippocampus Kindling, Neurologic Male Monosaccharide Transport Proteins Rabbits Rats Rats, Sprague-Dawley

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