Figure 9.

A schematic model of the development of Bax KO neurons after the elimination of PCD. In wild-type animals (A), excess MNs are eliminated from competition during the PCD period, so that the remaining MNs can now obtain sufficient trophic support for normal growth and survival. In contrast, because excess MNs in Bax KO mice (B) survive and compete for trophic support, the growth of all of the MNs is initially retarded. However, as a result of increasing limb size, the excess MNs whose axonal growth is slower than that of normal MNs lose contact with targets, which causes them to atrophy. As a consequence of the loss of competition from the excess MNs, the remaining MNs grow, differentiate normally, and maintain synaptic contact with the target. Postnatal treatment with GDNF (C) is able to rescue MNs from atrophy and loss of innervation.