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This book sets out to explain the clinically relevant basic mechanisms of excitotoxic neuronal death, which in the adult mammalian brain is morphologically necrotic, not apoptotic, and which involve caspase-independent mechanisms of programmed cell death.

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 (Siejo 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,...