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Purpose: Following stimulation of the main input to the hippocampus, the perforant pathway, in awake rats for 8 h, a seizure-free “latent period” is observed that lasts around three weeks. Continuous recording during the latent period from the dentate gyrus revealed spontaneous events that resembled low-frequency perforant pathway stimulation (PPS). This led us to hypothesize that, during the latent period, input from the entorhinal cortex kindles the hippocampus, eventually culminating in epilep-sy. We sought to test this hypothesis by removing entorhinal cortex input to the hip-pocampus immediately after pro-epileptogenic PPS.
Method: Male Sprague-Dawley rats received bilateral PPS lasting 8 h, which induces temporal lobe epilepsy and classic hippocampal sclerosis. Immediately after PPS, bi-lateral mechanical transection of the performant pathway was performed with a mi-croknife. Recording electrodes were re-implanted in the dentate gyrus and animals were continuously video-EEG monitored for spontaneous seizures, beginning two weeks after PPS. Longterm neuropathology was examined histologically starting sev-enty days after PPS. Controls were treated identically, but received sham surgery (skull trephination, no microknife insertion, recording electrode reimplantation, video-EEG monitoring).
Results: Bilateral angular bundle transection did not alter either epileptogenesis, e.g. the latency to epilepsy, or hippocampal neuropathology.
Conclusion: These data demonstrate that removing entorhinal cortex input to the hippocampus is not an effective antiepileptogenic treatment. Furthermore, this does not support the hypothesis that the entorhinal cortex is an epileptogenic zone that kindles the hippocampus during the latent period.