Fig. 9

Model of caspase-dependent cell death which occurs following neonatal hypoxia-ischemia (H-I). BAX likely plays a role in modulating caspase-3 activation via translocation to the mitochondria, release of cytochrome c, apoptosome formation, and activation of caspase-9 and -3. Caspase-8 activation may contribute to apoptotic-like death following neonatal H-I, as occurs in vitro and other paradigms, via BAX-dependent and independent pathways. How caspase-8 becomes activated in the neonatal brain has not yet been clarified. It is likely to occur via activation of a death receptor such as FAS or a member of a member of the TNF receptor family.