Denson G. Fujikawa 2+ In the early 1980s it was recognized that excessive Ca influx, presumably through 2+ 2+ voltage-gated Ca channels, with a resultant increase in intracellular Ca , 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 2+ hypoglycemia, energy failure was thought to be the reason for excessive Ca influx, whereas in status epilepticus it was thought that repetitive depolarizations were responsible (Siejö 1981). Meanwhile, John Olney found