Expression of Activating Transcription Factor 3 and Growth-associated Protein 43 in the Rat Geniculate Ganglion Neurons after Chorda Tympani Injury

Abstract

The purpose of this study was to evaluate the degree of damage in the geniculate ganglion and its target organ as a result of chorda tympani (CT) injury. We performed unilateral transection of the rat CT and examined expression of the activating transcription factor 3 (ATF3), a neuronal injury marker, and the growth-associated protein 43 (GAP-43), a regeneration-associated molecule. The mean proportion of ATF3-immunoreactive (ir) neurons in the geniculate ganglion was: 32% at 3 days after CT injury, but these neurons were never detected in the naive ganglion. Using in situ hybridization, the mean percentage of GAP-43 mRNA-labeled neurons (signal: noise ratio &#83 10) was observed to have increased significantly to 60% for 1-7 days after CT injury, while that in the naive ganglion was <15%. The results of morphological studies using scanning electron microscopy and immunohistochemistry indicated that atrophic change and reduction of protein gene-product 9.5-ir fibers in the denervated papillae, mainly in the intragemmal region, were observed after CT injury. Increase in GAP-43 mRNA, suggesting CT axonal regeneration, may have a role in recovery from taste disorders. However, this regenerative process may be involved in abnormal activity in the axotomized neurons or the adjacent intact neurons and so one must not disregard the existence of injured geniculate ganglions when considering the treatment of diseases that cause CT injury.

• Abnormal
• Activity
• Axotomized
• Neurons
• Denervation
• Intact
• Neurons
• Regeneration