Abstract
The mouse strain C57BL/6 suffers from the early onset of deafness. The deafness is attributable to sweeping degeneration of hair cells and the auditory nerve. Degeneration advances with age from the base to the apex of the cochlea. In the present study, neuronal condition was determined by linking relative levels of neuron specific enolase (NSE) in spiral ganglion neurons to their cytological appearances. NSE is an enolase isoform that is expressed only in nervous tissue and neuroendocrine glands.Mice ranged in age from 3 days to 10 months. Inner ears were fixed with 2.5% paraformaldehyde in 0.1 M cacodylate buffer, decalcified for 24 hrs with EDTA, and then embedded in either paraffin or polyester wax. The latter, which melts at a lower temperature, caused much less neuronal shrinkage during routine processing. Deparaffinized sections were exposed first to rabbit anti-bovine NSE antibodies, then to biotinylated swine anti-rabbit antibodies, and finally to peroxidase-labelled avidin.
Publisher
Cambridge University Press (CUP)
Reference8 articles.
1. This research was sponsored in part by grants from the Deafness Research Foundation, American Hearing Research Foundation, and Holmes Regional Medical Center, Melbourne, FL. The research was conducted at the Florida Institute of Technology, Melbourne, FL 32901. Ms. Susan Bullers assisted in the research.
2. Experimental Brain Ischemia: Neuron-Specific Enolase Level in Cerebrospinal Fluid as an Index of Neuronal Damage
3. Comparison of demyelination and neural degeneration in spiral and Scarpa's ganglia of C57BL/6 mice
4. DEVELOPMENT AND DEGENERATION OF HEARING IN THE C57/b16 MOUSE