Abstract \ud Temporal lobe epilepsy (TLE) is the most common partial epilepsy. Therefore, it is crucial to understand the mechanisms that contribute to the development of chronic TLE. It was generally believed that neurogenesis took place only during brain development, until in recent years proliferating cells were identified in the hippocampal dentate gyrus and olfactory bulb, providing compelling evidence that neurogenesis still occurs during adult life. Interestingly, studies have shown that seizure activity affects cell proliferation in animal models, proposing that it may potentially be involved in epileptogenesis. As yet, several studies have addressed this issue, yielding contradicting results. It has been demonstrated in animal seizure models that during the acute phase, neurogenesis briefly increases, subsequently decreasing in the chronic phase. Accumulating evidence suggests that neurogenesis does not play an essential role in epileptogenesis in adult rodents. Interestingly, age and/or disease related changes have been implicated in modifying the hippocampal environment so it no longer supports or promotes neurogenesis. Further, studies have shown that status epilepticus induction elicits a different response in the immature hippocampus, implying that in pups aberrant neurogenesis may play a more important role in epileptogenesis. Therefore, it should be determined whether neurogenesis is aberrant following seizures in rat pups and if it has long-term effects on the development of chronic seizures
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