ABSTRACT
At the outset it is acknowledged that this review accepts the common view that many forms of extraordinary CNS neuronal death, from transient ischemia, mild mechanical or pharmacological trauma, result from variants of excitatory amino acid (EAA) toxic causality. Specifically these conditions may arise from local and transient ischemic events or more widespread occurrences such as moderate head trauma or brief cardiac arrest. This set of conditions comprises a group that inflicts great social cost; and, in cases where there is an extended survival time course of neurons, the possibility of effective rescue exists. It has often been assumed, or implied, that a “one size fits all” model applies to all neuronal death ascribed to EAA toxicity. However, the present review emphasizes the view that immediate (within a few hours) and delayed (1-4 days) neuronal death should be viewed as having different, but perhaps, sequential etiologies. Olney and colleagues55,68 are primarily responsible for formulating the initial model of cell damage following excessive EAA
stimulation, and the work has spawned a great diversity of detailed models of the cascades leading to cell death.
