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Journal of Neuroscience, Vol 4, 1639-1652, Copyright © 1984 by Society for Neuroscience
Cell death of motoneurons in the chick embryo spinal cord. IX. The loss of motoneurons following removal of afferent inputs
N Okado and RW Oppenheim
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.
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