Abstract
Purpose: :
Previous studies showed that loss of muscarinic parasympathetic activation to the lacrimal gland (LG) leads to a dramatic reduction in tear secretion and atrophic changes to LG structure. Furthermore, apoptosis–related gene expression was found to be upregulated by microarray analysis. The purpose of this study was to determine the level of apoptosis in the experimental lacrimal gland.
Methods: :
Male Long–Evans rats underwent unilateral pre–ganglionic parasympathetic section of the greater superficial petrosal nerve (GSPN), the input to the pterygopatlatine ganglion. Clinical observations and Schirmer’s tear tests (STT) were performed prior to and post operatively. After 7 days, the animals were sacrificed and the lacrimal glands were removed for study. Structural changes in LG were examined by light microscopy. Apoptosis was detected by TUNEL assay kit (Roche).
Results: :
The STT values in the eye after section of the GSPN were significantly decreased (5.3±0.4mm, p<0.005, n=8) compared to the wetting levels in contra–lateral control eyes (9.1±1.8mm, n=8). Fluorescein scores (1.25±0.71) in the after GSPN section eye increased significantly, p<0.005, compared to the contra–lateral eye (2.88±0.35). Microscopic observation, revealed atrophic and fibrotic changes in LG after GSPN section. Furthermore, the number of TUNEL positive sites detected in LG after GSPN denervation increased significantly, and these were primarily in the periphery of acinii, between lobes, and were probably myoepithelial and basal cells.
Conclusions: :
These results suggest that loss of parasympathetic neuronal signaling results in atrophic changes in LG after parasympathetic denervation and that apoptosis is probably the underlying mechanism.
Keywords: lacrimal gland • innervation: neural regulation • apoptosis/cell death