The kainic acid model of temporal lobe epilepsy has greatly contributed to the understanding of the molecular, cellular and pharmacological mechanisms underlying epileptogenesis and ictogenesis. This model presents with neuropathological and electroencephalographic features that are seen in patients with temporal lobe epilepsy. It is also characterized by a latent period that follows the initial precipitating injury (i.e., status epilepticus) until the appearance of recurrent seizures, as observed in the human condition. Finally, the kainic acid model can be reproduced in a variety of species using either systemic, intrahippocampal or intra-amygdaloid administrations. In this review, we describe the various methodological procedures and evaluate their differences with respect to the behavioral, electroencephalographic and neuropathological correlates. In addition, we compare the kainic acid model with other animal models of temporal lobe epilepsy such as the pilocarpine and the kindling model. We conclude that the kainic acid model is a reliable tool for understanding temporal lobe epilepsy, provided that the differences existing between methodological procedures are taken into account.
Keywords: Animal models of temporal lobe epilepsy; Intracerebral administration; Kainic acid; Systemic administration.
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