In the early 1980s it was recognized that excessive Ca2+ influx, presumably through voltage-gated Ca2+ channels, with a resultant increase in intracellular Ca2+, was associated with neuronal death from cerebral ischemia, hypoglycemia, and status epilepticus (Siejö 1981). Calcium activation of phospholipases, with arachidonic acid accumulation and its oxidation, generating free radicals, was thought to be a potential mechanism by which neuronal damage occurs. In cerebral ischemia and hypoglycemia, energy failure was thought to be the reason for excessive Ca2+ influx, whereas in status epilepticus it was thought that repetitive depolarizations were responsible (Siejö 1981).
KeywordsCerebral Ischemia Status Epilepticus Neuronal Death Kainic Acid Monosodium Glutamate
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