Drug-resistant mesial temporal lobe epilepsy with hippocampal sclerosis is associated with anatomical, ultrastructural and functional changes that facilitate generation and spread of epileptic seizures. Intrahippocampal circuits are modified in their transversal lamellar and longitudinal translamellar organization. Neuronal death and the neuroplasticity of surviving cells contribute to major phenomena: an increased hyperexcitability of the hippocampal formation and an increased synchronization of its principal cells. Selective disruption of the epileptic networks that are involved in mesial temporal lobe epilepsy may have a therapeutic effect. We present here the preliminary results of a selective intrahippocampal transection in a chronic model of mesial temporal lobe epilepsy after focal injection of kainic acid in adult mice. A complete transection of the hippocampal formation (including dentate gyrus and hippocampus proper, sparing the fimbria) results in a blockade of ictal activities spread from the generator, a reduction in their frequency and an increase in their duration. In contrast, after a transection sparing the dentate gyrus and hilus, no modification was noted. In this model of mesial temporal lobe epilepsy, longitudinally projecting axonal circuits of the dentate gyrus and hilus appear to be implicated in generation, propagation and interruption of ictal activities within hippocampal formation.