Y. Li et G. Raisman, SPROUTS FROM CUT CORTICOSPINAL AXONS PERSIST IN THE PRESENCE OF ASTROCYTIC SCARRING IN LONG-TERM LESIONS OF THE ADULT-RAT SPINAL-CORD, Experimental neurology, 134(1), 1995, pp. 102-111
Small, circumscribed electrolytic lesions were made in the corticospin
al tract at the upper cervical level of the adult rat spinal cord. At
increasing survival times, immunohistochemistry of glial fibrillary ac
idic protein and electron microscopy showed that the predominantly lon
gitudinal astrocytic processes underwent a progressive hypertrophy, wh
ich spread from the lesion, increasing in intensity from 1 week and re
aching a maximum at between 9.5 and 13 weeks, by which time the lesion
was completely surrounded by a dense astrocytic scar. A previous stud
y 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 c
ut axons, and also the adjacent uncut axons, emitted extensive arboriz
ations of sprouts directed into the central, macrophage-filled area of
the lesion. The present experiments indicated that the axon sprouts p
ersisted apparently undiminished over the period (from 9.5 to 13 weeks
) when the astrocytic scarring process was reaching its maximum. Surro
unding the center of the lesion was an area in which the axons had bec
ome demyelinated. By 3 weeks a few axons were remyelinated with periph
eral myelin formed by Schwann cells which had migrated into the lesion
s. 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 t
erminal expansions, which were sheathed, but not myelinated, by satell
itic Schwann cells. Thus, at survivals long enough for the formation o
f a dense, astrocytic scar, cut corticospinal axons retain extensive t
erminal and collateral arborizations even in the macrophage-filled cen
tral lesion area and are myelinated or ensheathed by endogenous Schwan
n cells. (C) 1995 Academic Press, Inc.