Bcl-xL, on the other hand, may be crucial for the survival
of neurons during embryonic development. Mice deficient
in bcl-xL die early during embryogenesis, probably due to
massive cell death occurring in the developing nervous system
(Motoyama et al., 1995). While endogenous Bcl-xL is
important in the control of developmental neuronal apoptosis,
the overexpression of Bcl-xL in neurons in transgenic
mice results in resistance to apoptosis triggered by axotomy
and hypoxia-ischemia