Two groups have utilized molecular genetic approaches to examine the
role of caspases in neurotrophin withdrawal-induced programmed cell
death. Friedlander et al. observed diminished cell death 24 h after neutrophin
withdrawal from dorsal root ganglion neurons of caspase-1–/– mice or mice
expressing a dominant negative caspase-1 inhibitor as compared to wildtype
litter mates.178 Because a single time point was examined, it is unclear
whether caspase-1 inhibition actually prevented neuronal apoptosis or
merely slowed the kinetics. Consistent with the latter hypothesis, mice from
these animals were viable and did not display supernumerary neurons or
developmental abnormalities.178 These results suggest that caspase-1 might
play a critical role in apoptosis induced by postnatal neutrophin withdrawal
but not prenatal (developmental) apoptosis