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Original Article

Glial Reaction after Facial Nerve Compression in the Facial Canal of the Albino Rat

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Pages 271-277 | Received 05 Aug 1993, Accepted 26 Oct 1993, Published online: 08 Jul 2009
 

Abstract

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% periodate-lysine-paraformaldehyde fixative. Frozen sections from the brain stem containing the facial motor nucleus (FMN) were obtained and stained for OX-42 (against CR3 antigen), OX-18 (against Class I MHC antigen), OX-6 (against Class II MHC antigen) and GFAP (anti-glial fibrillary acidic protein). The first glial reaction in the FMN occurred in the microglia which showed a significant increase in the CR3 immunoreactivity within 24 h after compression. Upregulation of the GFAP was not noticed until 2 days after compression. In each case, the staining reaction 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 increased and was most likely the result of proliferation of the resident microglia rather than invasion from the blood stream. The increase in the number of GFAP positive cells was most likely the result of more resident astrocytes being activated, as previous studies have shown the absence of mitotic activity of astrocytes after lesion of the facial nerve. In addition to increased CR3 and GFAP activity there was also an upregulation of Class I MHC antigen in the microglia, as revealed by increased immunostaining against OX-18. This began to appear at day I 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 FMN, indicating that there was no detectable change in the class II MHC activity.

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