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Excerpt
Peripheral facial nerve paralysis associated with taste disturbances is often encountered in clinical practice. In this study, we attempt to explain the mechanism inducing and maintaining this gustatory function by focusing on geniculate ganglion cells.
Methods
We created a rat model of peripheral facial nerve (chorda tympani) paralysis under deep anesthesia. Using an operating microscope, the maxillary artery was exposed and cannulated with a polyethylene catheter, and an injection of embolizing material was given via the catheter. We observed the changes in the facial nerve in the temporal bone after embolization, using confocal laser scanning microscopy and in situ hybridization histochemistry. Gene expression was measured with a computerized image analysis system.
Results
Complete paralysis of the facial nerve occurred 5 to 15 minutes after embolization. Degenerative changes were seen in 6.8-7.5% of nerve fibers. There were several microspheres in the horizontal portion of the facial nerve on the operated side. Avascular areas close to the trapped site were visible, but the rest of the capillaries appeared normal. The expression of SP and trkB mRNA decreased 1 day after embolization, lasted for 2 weeks, and gradually recovered. GAP-43 mRNA increased 3 days after the operation, and remained elevated for at least 2 weeks.
Conclusions
The results suggest that SP, trkB, and GAP-43 expression in the geniculate ganglion is affected by injury to the chorda tympani nerve in this model, and may result in functional alteration of the taste receptors.
