Ok, sure, we could call it neuroptocrosis. Good a name as any. Sometimes I like
to call it ischemic neurolysis. Some people just call it ischemic
neuronal death. Either way, what we're talking about is a spectrum
of cell death phenotypes initiated by ischemia. We've seen, for example, how
extremely complex interactions between Bcl-2 proteins can lead to varying
outcomes--like the outcome of a throw of the dice or a chaotic shootout in Tombstone. We've
seen how the Four Horsemen interact with each other. Which one is more
responsible for cell death? Nobody can answer that question.
And so one could make the argument that the final death
phenotype--classically apoptotic or classically necrotic--is not nearly as
important as important as the lethal events that occur early in ischemia--loss
of high energy phosphate, surges in glutamate, Ca2+ flux, elaboration of
reactive oxygen species, activation of proteases, phosphorylation of eIF2α, and
interruption of translation initiation. And the ultimate death phenotpe is not
as important as as events that come some time later--dysfunction of organelles,
abnormal genetic responses, calpain-mediated proteolysis, release of cytochrome
c, and complex Bcl-2 interactions.
We do know that, given a particular insult, a given
population of cells will usually assume a particular range of death phenotypes.
But I think this is a little like knowing that, given a particular set of
circumstances, a storm will probably brew today and not tomorrow, or an electron will probably be here and not there. As
with the weather pattern and the electron's position, the final fate of a particular cell after a
particular insult isn't so much a deterministic fate as a statistical one.