OBJECTIVE: Patients with temporal lobe epilepsy often display cognitive 
comorbidity with recurrent seizures. However, the cellular mechanisms underlying 
the impairment of neuronal information processing remain poorly understood in 
temporal lobe epilepsy. Within the hippocampal formation neuronal networks 
undergo major reorganization, including the sprouting of mossy fibers in the 
dentate gyrus; they establish aberrant recurrent synapses between dentate 
granule cells and operate via postsynaptic kainate receptors. In this report, we 
tested the hypothesis that this aberrant local circuit alters information 
processing of perforant path inputs constituting the major excitatory afferent 
pathway from entorhinal cortex to dentate granule cells.
METHODS: Experiments were performed in dentate granule cells from control rats 
and rats with temporal lobe epilepsy induced by pilocarpine hydrochloride 
treatment. Neurons were recorded in patch clamp in whole cell configuration in 
hippocampal slices.
RESULTS: Our present data revealed that an aberrant readout of synaptic inputs 
by kainate receptors triggered a long-lasting impairment of the perforant path 
input-output operation in epileptic dentate granule cells. We demonstrated that 
this is due to the aberrant activity-dependent potentiation of the persistent 
sodium current altering intrinsic firing properties of dentate granule cells.
INTERPRETATION: We propose that this aberrant activity-dependent intrinsic 
plasticity, which lastingly impairs the information processing of cortical 
inputs in dentate gyrus, may participate in hippocampal-related cognitive 
deficits, such as those reported in patients with epilepsy.