Sprouts from cut corticospinal axons persist in the presence of astrocytic scarring in long-term lesions of the adult rat spinal cord.
Small, circumscribed electrolytic lesions were made in the corticospinal tract at the upper cervical level of the adult rat spinal cord. At increasing survival times, immunohistochemistry of glial fibrillary acidic protein and electron microscopy showed that the predominantly longitudinal astrocytic processes underwent a progressive hypertrophy, which spread from the lesion, increasing in intensity from 1 week and reaching a maximum at between 9.5 and 13 weeks, by which time the lesion was completely surrounded by a dense astrocytic scar. A previous study with orthograde transport of axonal tracers showed that from 2 weeks after the lesion the main axonal stems of both cut and adjacent uncut corticospinal axons had large varicosities. The swollen ends of the cut axons, and also the adjacent uncut axons, emitted extensive arborizations of sprouts directed into the central, macrophage-filled area of the lesion. The present experiments indicated that the axon sprouts persisted apparently undiminished over the period (from 9.5 to 13 weeks) when the astrocytic scarring process was reaching its maximum. Surrounding the center of the lesion was an area in which the axons had become demyelinated. By 3 weeks a few axons were remyelinated with peripheral myelin formed by Schwann cells which had migrated into the lesions. By 4 months the scar region was densely colonized by Schwann cells, which now had remyelinated a wide swath of both cut and uncut axons. The cut axons were myelinated by Schwann cells as far as their large terminal expansions, which were sheathed, but not myelinated, by satellitic Schwann cells. Thus, at survivals long enough for the formation of a dense, astrocytic scar, cut corticospinal axons retain extensive terminal and collateral arborizations even in the macrophage-filled central lesion area and are myelinated or ensheathed by endogenous Schwann cells.
Li
Y
Y
Norman and Sadie Lee Research Centre, National Institute for Medical Research, London United Kingdom.
Raisman
G
G
D000818:Animals; D001253:Astrocytes / Q000473:pathology*; D001369:Axons / Q000502:physiology*; D002921:Cicatrix / Q000473:pathology*; D003714:Denervation; D005260:Female; D008854:Microscopy, Electron; D009416:Nerve Regeneration; D011712:Pyramidal Tracts / Q000502:physiology* / Q000648:ultrastructure; D051381:Rats; D011919:Rats, Inbred Strains; D013118:Spinal Cord Diseases / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors