Abstract
Functional and molecular changes in glutamate transporters during kindling epileptogenesis were investigated in hippocampus CA1-region of rats. In control animals total glutamate transporter activity was indicated by the stimulatory effect of the high-affinity transporter blocker l- trans-pyrrolidine-2,4-dicarboxylate on extracellular glutamate and aspartate concentrations, as measured by in vivo microdialysis. This blocker-induced elevation was absent already early during epileptogenesis. CA1 levels of the glutamate transporter subtypes GLAST and GLT-1, analyzed by quantitative immunoblotting, did not change during kindling epileptogenesis. However, the 60% decrease in EAAC-1 level observed in age-matched controls was fully compensated for in kindled animals 4–5 weeks after the last generalized seizure. These results indicate a compensatory change of the neuronal EAAC-1 glutamate transporter in CA1 region during kindling epileptogenesis, which may be the consequence of a decrease in total transporter activity.
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