The chronic effects of the lesioning agent, kainic acid, on paired pulse inhibition in the CA1 area were investigated in the hippocampus both in vivo and in vitro. Pretreatment of animals with a unilateral intracerebroventricular (i.c.v.) injection of kainic acid resulted in a lesion of the CA3/4 area of the hippocampus ipsilateral to the injection site. On activating the surviving Schaffer collateral afferents in the contralateral hippocampus, normal paired-pulse inhibition of the extracellularly recorded population spike in CA1 was observed. On activating the surviving commissural afferents to the CA1 area ipsilateral to the lesion, no such inhibition could be observed. However, paired-pulse inhibition was recorded in the dentate gyrus ipsilateral to the lesion in response to stimulation of the perforant path. The chronic failure of inhibition following the unilateral i.c.v. injection of kainic acid further supports the use of this method to provide a chronic model in the rat for the study of epileptogenesis in the hippocampus.