Rs. Ruan et al., GLIAL REACTION AFTER FACIAL-NERVE COMPRESSION IN THE FACIAL CANAL OF THE ALBINO-RAT, Acta oto-laryngologica, 114(3), 1994, pp. 271-277
The facial nerve of the albino rat was compressed by inserting a thin
nylon thread in the facial canal. After a survival period of 1-60 days
, the animal was perfused with Ringer's solution followed by a 2% peri
odate-lysine-paraformaldehyde fixative. Frozen sections from the brain
stem containing the facial motor nucleus (FMN) were obtained and stai
ned for OX-42 (against CR3 antigen), OX-18 (against Class I MHC antige
n), OX-6 (against Class II MHC antigen) and GFAP (anti-glial fibrillar
y acidic protein). The first glial reaction in the FMN occurred in the
microglia which showed a significant increase in the CR3 immunoreacti
vity within 24 h after compression. Upregulation of the GFAP was not n
oticed until 2 days after compression. In each case, the staining reac
tion was initially light, but increased with time and appeared to peak
at 3-4 days for OX-42 and 4-5 days for GFAP. The activated microglia
first assumed a perineuronal position but were later displaced by the
activated astrocytes. The number of stained microglia was noticeably i
ncreased and was most likely the result of proliferation of the reside
nt microglia rather than invasion from the blood stream. The increase
in the number of GFAP positive cells was most likely the result of mor
e resident astrocytes being activated, as previous studies have shown
the absence of mitotic activity of astrocytes after lesion of the faci
al nerve. In addition to increased CR3 and GFAP activity there was als
o an upregulation of Class I MHC antigen in the microglia, as revealed
by increased immunostaining against OX-18. This began to appear at da
y 1 postoperation and increased with time till it peaked at about 5-6
days postoperation. Many of them like OX-42 positive cells, occupied a
perineuronal position. No OX-6 positive cells were detected in the FM
N, indicating that there was no detectable change in the class II MHC
activity.