PMC:3312845 / 1830-2797 JSONTXT

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SE has been defined as continuous seizure activity, which causes neuronal cell death, epileptogenesis and learning impairment [2,3]. Some brain regions vulnerable to SE play a role in the generation and propagation of paroxysmal activity in experimental epilepsy models. The piriform cortex (PC) is one of the most susceptible brain regions to seizure-induced damage in the kainate, pilocarpine and other models of temporal lobe epilepsy (TLE) [4-6]. Pilocarpine, a cholinergic agonist, induces SE in rodents. This pilocarpine-induced SE, similar to human TLE, shows massive neuronal loss in the hippocampus followed by glial proliferation. This neuronal damage in the pilocarpine model is not restricted to the hippocampus, but often extends to extrahippocampal limbic structures. Indeed, pilocarpine-induced SE results in acute neuronal damages within layers II and III of the PC [5,6]."}

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epilepticus (SE) is a medical emergency with significant mortality [1]. SE has been defined as continuous seizure activity, which causes neuronal cell death, epileptogenesis and learning impairment [2,3]. Some brain regions vulnerable to SE play a role in the generation and propagation of paroxysmal activity in experimental epilepsy models. The piriform cortex (PC) is one of the most susceptible brain regions to seizure-induced damage in the kainate, pilocarpine and other models of temporal lobe epilepsy (TLE) [4-6]. Pilocarpine, a cholinergic agonist, induces SE in rodents. This pilocarpine-induced SE, similar to human TLE, shows massive neuronal loss in the hippocampus followed by glial proliferation. This neuronal damage in the pilocarpine model is not restricted to the hippocampus, but often extends to extrahippocampal limbic structures. Indeed, pilocarpine-induced SE results in acute neuronal damages within layers II and III of the PC [5,6]."}

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