Cell death of motoneurons in the chick embryo spinal cord. IX. The loss of motoneurons following removal of afferent inputs.

The primary aim of this study was to clarify the role of supraspinal, propriospinal, and primary sensory afferents in motoneuron (MN) development in the lateral motor column (LMC) of the lumbar spinal cord of the chick embryo. For this purpose three types of operations were carried out on embryonic day (E) 2. (1) The spinal cord was transected at the cervical (C-gap) or at the thoracic (T-gap) level so as to eliminate supraspinal and/or propriospinal inputs to the lumbar cord. (2) The entire lumbar neural crest was removed (NCR) in order to eliminate primary sensory inputs arising from the dorsal root ganglia (DRG). (3) A combined operation of T-gap and lumbar NCR was performed. The numbers of MNs in the LMC of the lumbar spinal cord were counted in embryos sacrificed between E10 and E18. The number of MNs on E10, when naturally occurring neuron death is almost complete, was not changed following either operation 1 or 2 described above. However, by E16, when naturally occurring neuron death is over, these same deafferented groups had 20 to 25% fewer MNs than did controls. Thus, the removal of either descending or sensory (DRG) afferents results in a significant increased loss of MNs that appears to take place only during the final stages of natural neuronal death or later. By contrast, the removal of both sources of input (T-gap + NCR) results in an additional 37% loss of MNs by E10 compared to controls. Thus, in this group deafferentation significantly increases cell loss during the major period of naturally occurring MN death (E5 to E10). No further loss of MNs occurs in this group after E10. Chronic treatment of deafferented embryos with curare from E6 to E9 or from E10 to E14 prevented the naturally occurring MN loss during these stages but was without effect on the increased cell loss induced by deafferentation. These results imply that the cellular mechanisms involved in target- versus afferent-regulated cell death are different. Collectively, these results indicate that the regulation of MN numbers is more complicated than previously thought. Both targets and afferents appear to be involved in controlling the survival of this population of neurons during the period of naturally occurring MN death.