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.