(Oppenheim, 1991). There is growing evidence, however, that Colman, 1993). Survival of newly formed oligodendrocytes in

culture can be promoted by growth factors produced by their tion of the commissural axon tracts. Glial apoptosis is blocked in embryos deficient for reaper, where greater than expression of the rhomboid gene, without changing axon number. Extra MGA and MGM were eliminated from the o 8glial cell number is also regulated by differential cell prolifer-ation and cell death, leading to speculation that glial cell number may be regulated by mechanisms similar to those described for neuronal cell number (Raff et al., 1993). In some neuronal populations, cell death results from the matching of cells to their efferent targets and is believed to operate by a trophic mechanism (Hamburger and Oppenheim, 1982). The deletion of targets result in reductions in the survival of the innervating population of neurons (Oppenheim, 1985; Hamburger and Oppenheim, 1982). Considerable evidence indicates that trophic support may also originate from afferent inputs, glia and the extracellular matrix (Okado an