CELL DAMAGE/EXCITOTOXICITY
Many studies have demonstrated the occurrence of neuronal cell death through necrosis, apoptosis, or other forms of programmed cell death (PCD) in a number of models of status epilepticus (SE). Significant age-related, model-dependent, and regional differences in the vulnerability to, and in the mechanisms of, PCD have been recognized. In some models like the lithium-pilocarpine (LiPC), corticotrophin-releasing hormone, and the homocysteic acid rodents, the developing brain is more likely (compared to the mature brain) to manifest apoptosis. In other models, such as perforant path stimulation, flurothyl inhalation, and hyperthermia, necrosis with or without apoptosis has been observed in the immature brain. Although there is some evidence that PCD in the developing brain, like in the adult brain, may involve activation of p53- and ceramide-related pathways, the mechanisms of seizure-related PCD – which have extensively been studied in adult animals – still remain to be fully investigated in the developing animals.