Adult mice and rats were sacrificed by perfusion between 2 and 90 days
after right pyramidotomy to study the microglial and astroglial respo
nse in the brain and spinal cord. The microglia were detected immunohi
stochemically with OX-42, OX-18 and OX-6 to assess respectively the ex
pression of complement type 3 receptor, and major histocompatibility c
lass I and class II antigens. Cell counting was also carried out in so
me animals to determine the possible proliferation of glial cells in t
he corticospinal tract and around layer V neurons in the cerebral cort
ex. Some operated animals were given rhodamine B isothiocyanate inject
ion to investigate whether macrophages/monocytes could have migrated f
rom the blood stream to the reactive area. The glial response around t
he cell bodies of layer V neurons in the ipsilateral cerebral cortex d
id not display any noticeable difference compared with that of the con
tralateral side and of the cerebral cortex of the sham-operated and no
rmal control animals. In the cervical and lumbar cord segments of the
operated animals, reactive microglial cells in the contralateral corti
cospinal tract appeared as early as 2 days post pyramidotomy (PP) in r
ats and 4 days PP in mice. Activation of microglial cells lasted up ti
ll 35 days PP, showing gradual increase in immunoreactive staining and
hypertrophy After that, the microglial immunoreactivity subsided and
the cells assumed normal appearance by 90 days PP. Quantitative analys
is showed a marked increase in the number of microglial cells in the c
ontralateral CST up till 60 days PP. In mice, at 6 days PP, astroglial
cells were hypertrophic and more intensely stained but showed no incr
ease in number. No noticeable changes were noted in the astroglia of t
he rats throughout the period studied. Rhodamine-labelled cells were f
ound at the lesion site, but not in layer V of the cerebral cortex, no
r in the corticospinal tract. Though different glial reactions in the
degenerating corticospinal tract were noted in mice and rats, there wa
s the same apparent lack of glial reaction around the cell bodies of l
ayer V neurons in the two animal species. Such lack of significant gli
al response is different from the vigorous glial response around the c
ell bodies of peripherally projecting neurons demonstrated in previous
work. The possible mechanisms for such difference and the implication
of the difference in axonal regeneration were discussed. (C) 1995 Aca
demic Press Limited.