title: An in vivo quantifiable model of cochlear neuronal degeneration induced by central process injury.
abstract: In the available in vivo experimental models for cochlear neuronal degeneration, the peripheral (hair cell side) process of the cochlear nerve has been injured in order to induce neuronal degeneration. However, there has been no dependable experimental model in which cochlear neuronal degeneration begins from the central (brain stem side) process. This lack of a central process injury model has probably been due to the experimental difficulties that had to be overcome in order to reproducibly and selectively injure the central process of the cochlear neurons while maintaining the patency of the internal auditory artery in small experimental animals such as rats. Using rats, we first developed a central process injury model in which the reduction of the spiral ganglion cells due to retrograde degeneration of cochlear neurons can be quantitatively evaluated. In our experimental model, the cochlear nerve was compressed and injured by a compression-recording (CR) electrode placed at the internal auditory meatus. First, the cochlear nerve was compressed until the compound action potentials of the cochlear nerve became flat, and then the CR electrode was advanced by various compression speeds (5, 10, or 200 micrometer/s) to reach the same depth (400 micrometer). In our model, therefore, the reduction of the spiral ganglion cells was caused compression speed dependently. This method made it possible to produce compression injury to the cochlear nerve without evidence of damage to the blood supply to the cochlea via the internal auditory artery. This model gives us the means to obtain knowledge that was previously impossible to derive from the peripheral process injury models.
authors.affiliation: Department of Neurosurgery, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, 036-8216, Japan.
authors.forename: T
authors.initials: T
authors.lastname: Sekiya
authors.forename: T
authors.initials: T
authors.lastname: Hatayama
authors.forename: N
authors.initials: N
authors.lastname: Shimamura
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D001306:Auditory Pathways / Q000473:pathology / Q000503:physiopathology; D001930:Brain Injuries / Q000473:pathology* / Q000503:physiopathology; D001933:Brain Stem / Q000473:pathology* / Q000503:physiopathology; D003056:Cochlear Nerve / Q000473:pathology* / Q000503:physiopathology; D004572:Electrolysis / Q000379:methods; D008297:Male; D009410:Nerve Degeneration / Q000473:pathology* / Q000503:physiopathology; D009474:Neurons / Q000473:pathology* / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013136:Spiral Ganglion / Q000473:pathology / Q000503:physiopathology