C. Kaur et al., THE EFFECTS OF SUBCUTANEOUS INJECTIONS OF GLUCOCORTICOIDS ON AMEBOID MICROGLIA IN POSTNATAL RATS, Archives of histology and cytology, 57(5), 1994, pp. 449-459
Subcutaneous injections of glucocorticoids into postnatal rats resulte
d in a drastic reduction in the number of amoeboid microglial cells in
the corpus callosum as shown by their labelling with the monoclonal a
ntibodies of the OX-series, ED1, lectin and rhodamine isothiocynate (R
hIc), In rats receiving 2 or 3 injections of glucocorticoids and kille
d at the age of 4 or 7 days, between 40 to 60% of the callosal amoeboi
d microglial cells were depleted when compared with the corresponding
control animals, The cells that survived the glucocorticoid treatments
became ramified, while those in the controls of the same age group re
mained round or amoeboidic, In rats killed at 2 or 3 weeks of age, the
microglia became extremely ramified with a concomitant diminution in
their immunostaining, particularly in the glucocorticoid-injected rats
. In rats receiving glucocorticoid injections along with RhIc, the RhI
e-laden amoeboid microglia appeared round and amoeboidic and were inte
nsely stained with OX-42, suggesting their activation and upregulation
of complement type 3 receptors when compared with rats receiving only
glucocorticoids, Compared with the control, cellular proliferation co
ntinued in rats given glucocorticoid injection as indicated by the occ
urrence of many bromodeoxyuridine-lakelled cells in the corpus callosu
m at the age of 6 days, Ultrastructural studies confirmed the presence
of mitotic cells identified as amoeboid microglia because of their la
belling with isolectin, A striking ultrastructural feature in glucocor
ticoids-injected rats was the wide occurrence of amoeboid microglial c
ells that had ingested a variable number of lectin-labelled cells, It
is concluded from this study that the drastic reduction of amoeboid mi
croglia after glucocorticoid injections can be attributed to the suppr
ession of their precursor cells, monocytes, Another possible explanati
on is the acceleration of their degeneration process, probably greatly
enhanced by glucocorticoids; the degenerating amoeboid microglia were
readily eliminated by the surviving amoeboid microglial cells through
endocytosis. Glucocorticoids also accelerated the maturation process
of the persisting amoeboid microglia to become ramified in form.