Increases in collateral axonal growth rostral to a thoracic hemisection in neonatal and weanling rat.
The spinal cords of newborn and weanling rats were hemisected at the mid-thoracic level. Control studies revealed that Fink-Heimer positive debris was absent in the gray matter at three months postoperative. The remaining animals were given a second lesion, a high cervical spinal hemisection, at five to seven months after the original thoracic hemisection. The pattern of degeneration rostal to the thoracic lesion was compared with similar regions of the spinal cord from animals receiving only a cervical hemisection at the adult stage. In neither experimental group of doubly hemisected rats was there any degeneration observed below the thoracic lesion site, even though no glial or connective tissue scar had formed in animals originally operated at birth. Thus no regeneration had occurred. At least one segment above the initial hemisection: 1. the majority of degenerating axons were localized toward the lateral edge of the spinal cord, especially in the doubly lesioned neonatal group; 2. the erae of ipsilateral white matter was reduced more in the neonatal than the weanling operates; 3. there was an upward shift in axonal diameter of ipsilateral fibers in both the region of the rubrospinal tract and the ventrolateral portion of the lateral funiculus of the doubly hemisected rats when compared with the cervically lesioned controls; 4. a significantly greater amount of degeneration was present in lamina VII of Rexed in both the neonatal and weanling experimental operates (p less than 0.05 weanling; p less than 0.001 neonate); 5. no mean difference in area was seen between the ipsilateral and contralateral gray matter in any group for the segments of the spinal cord in which the judgements and measurements were taken. These data suggest that there has been sprouting of axons from descending nerve tracts rostral to the thoracic lesion in both the neonatal and weanling experimental groups. The question remains whether the sprouting of descending nerve tracts is from collateral of axons which normally project rostral to the thoracic hemisection and are not cut by the thoracic lesion (collateral sprouting) or from collaterals of lesioned axons (regenerative sprouting). Present evidence favors collateral sprouting, expecially in the neonatal operate where much retrograde cell death appears to have taken place.
D000367:Age Factors; D000818:Animals; D000831:Animals, Newborn / Q000502:physiology*; D001369:Axons / Q000502:physiology* / Q000648:ultrastructure; D004525:Efferent Pathways / Q000502:physiology; D007839:Functional Laterality; D006614:Hindlimb / Q000294:innervation; D009186:Myelin Sheath / Q000648:ultrastructure; D009333:Neck; D009410:Nerve Degeneration; D009416:Nerve Regeneration; D051381:Rats; D013116:Spinal Cord / Q000502:physiology* / Q000648:ultrastructure; D013909:Thorax