Kindling is an animal model of epilepsy which involves a permanently enhanced neuronal response to an electrical stimulus. It has been proposed that long-term potentiation (LTP) of excitatory synaptic transmission is the cellular basis of kindling. Therefore, LTP was examined in the monosynaptic projections from the lateral entorhinal cortex (LEC) to dentate granule cells (DG) in unrestrained, unanesthetized rats kindled via the LEC. Population excitatory postsynaptic potentials (pEPSPs) were recorded from the granule cells before, during, and after kindling of the LEC. Controls were unkindled rats recorded during the same time period as the experimental rats. No consistent changes were found in plateau pEPSP amplitudes or initial slopes although kindling via the LEC proceeded through the typical stages. There was also no significant change in the stimulus intensity needed to elicit a 50% maximal or "plateau" pEPSP. Thus, whereas kindling was indeed established by stimulation of the LEC, there was no evidence of LTP detected in the granule cell response either during the development or after completion of kindling. Either LTP does not underlie the mechanism of kindling via this pathway or it occurs in different brain regions receiving LEC input.