I am building a numerical model of the neural activity after a stroke. My observation from the literature is that synapses fail typically ten seconds after interruption of blood flow. I found multiple hypotheses for this synaptic failure.
The most popular seems to be that a presynaptic rise in Ca concentration can lead to a diminished influx of Ca during an action potential, which normally triggers transmitter vesicle exocytosis. (There apparently needs to be a rise in concentration for the release?) Does someone have an idea if this is the case and maybe know of some published quantitative measurements on this?
Have you tried to read ? :
Konstantin-Alexander Hossmann. Pathophysiology and therapy of experi-
mental stroke. Cell Mol Neurobiol, 26(7-8):1057{1083, 2006.
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