Modifications of motoneuron development following transplantation of thoracic spinal cord to the lumbar region in the chick embryo: evidence for target-derived signals that regulate differentiation.
In order to examine the role of target cells in the development of spinal motoneurons, the neural tube from thoracic segments was transplanted to the lumbar region on embryonic day (E) 2, and allowed to innervate hindlimb muscles in the chick embryo. When examined at later stages of development, the proportion of white and gray matter in the thoracic transplant was altered to resemble normal lumbar cord. Many thoracic motoneurons were able to survive up to posthatching stages following transplantation. The branching and arborization of dendrites of thoracic motoneurons innervating hindlimb muscles, as well as motoneuron (soma) size, were also increased to an extent approximating that seen in normal lumbar motoneurons. In support of previous studies using a similar transplant model, we have also found that the peripheral (intramuscular) branching pattern of thoracic motoneuron axons innervating hindlimb muscles was similar to that of normal lumbar motoneurons. Axon size and the degree of myelination of transplanted thoracic motoneuron axons were also increased so that these parameters more closely resembled axons of normal lumbar than normal thoracic spinal motoneurons. Virtually all of the changes in motoneuron properties noted above were observed irrespective of whether or not the transplanted spinal cord had developed in anatomical continuity with the host rostral cord. Accordingly, it is unlikely that the changes in the development of transplanted thoracic motoneurons reported here are induced either entirely, or in part, by signals derived from the host central nervous system. Rather, these changes appear to be mediated by interactions between the transplanted motoneurons and the hindlimb. We favor the notion that retrograde trophic signals derived from the hindlimb act to modulate the development of innervating motoneurons. Whether this signal involves a diffusible trophic agent released from target cells, or acts by some other mechanism is presently unknown.
Yin
Q W
QW
Department of Neurobiology and Anatomy, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27157.
Oppenheim
R W
RW
D000818:Animals; D001369:Axons / Q000502:physiology / Q000648:ultrastructure; D002454:Cell Differentiation / Q000502:physiology; D002642:Chick Embryo; D003712:Dendrites / Q000648:ultrastructure; D016332:Fetal Tissue Transplantation; D007150:Immunohistochemistry; D008854:Microscopy, Electron; D009046:Motor Neurons / Q000502:physiology* / Q000648:ultrastructure; D009132:Muscles / Q000294:innervation; D009186:Myelin Sheath / Q000648:ultrastructure; D013116:Spinal Cord / Q000166:cytology / Q000502:physiology* / Q000637:transplantation; D014184:Transplantation, Homologous