title: Synaptic plasticity after chemical deafening and electrical stimulation of the auditory nerve in cats.
abstract: The effects of deafness on brain structure and function have been studied using animal models of congenital deafness that include surgical ablation of the organ of Corti, acoustic trauma, ototoxic drugs, and hereditary deafness. This report describes the morphologic plasticity of auditory nerve synapses in response to ototoxic deafening and chronic electrical stimulation of the auditory nerve. Normal kittens were deafened by neonatal administration of neomycin that eliminated auditory receptor cells. Some of these cats were raised deaf, whereas others were chronically implanted with cochlear electrodes at 2 months of age and electrically stimulated for up to 12 months. The large endings of the auditory nerve, endbulbs of Held, were studied because they hold a key position in the timing pathway for sound localization, are readily identifiable, and exhibit deafness-associated abnormalities. Compared with those of normal hearing cats, synapses of ototoxically deafened cats displayed expanded postsynaptic densities, a 35.4% decrease in synaptic vesicle (SV) density, and a reduction in the somatic size of spherical bushy cells (SBCs). In comparison with normal hearing cats, ototoxically deafened cats that received cochlear stimulation had endbulbs that expressed postsynaptic densities (PSDs) that were statistically identical in size, showed a 48.1% reduction in SV density, and whose target SBCs had a 25.5% reduction in soma area. These results demonstrate that electrical stimulation via a cochlear implant in chemically deafened cats preserves PSD size but not other aspects of synapse morphology. This determination further suggests that the effects of ototoxic deafness are not identical to those of hereditary deafness.
authors.affiliation: Department of Otolaryngology-HNS, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA. dryugo@jhu.edu
authors.forename: D K
authors.initials: DK
authors.lastname: Ryugo
authors.forename: C A
authors.initials: CA
authors.lastname: Baker
authors.forename: K L
authors.initials: KL
authors.lastname: Montey
authors.forename: L Y
authors.initials: LY
authors.lastname: Chang
authors.forename: A
authors.initials: A
authors.lastname: Coco
authors.forename: J B
authors.initials: JB
authors.lastname: Fallon
authors.forename: R K
authors.initials: RK
authors.lastname: Shepherd
mesh_terms: D000818:Animals; D000900:Anti-Bacterial Agents / Q000633:toxicity; D002415:Cats; D003056:Cochlear Nerve / Q000503:physiopathology* / Q000648:ultrastructure; D017626:Cochlear Nucleus / Q000503:physiopathology / Q000648:ultrastructure*; D003638:Deafness / Q000139:chemically induced / Q000503:physiopathology*; D004195:Disease Models, Animal; D004558:Electric Stimulation / Q000379:methods; D004567:Electrodes, Implanted; D016057:Evoked Potentials, Auditory, Brain Stem / Q000187:drug effects; D005260:Female; D008297:Male; D008854:Microscopy, Electron; D009355:Neomycin / Q000633:toxicity; D009411:Nerve Endings / Q000648:ultrastructure; D009473:Neuronal Plasticity; D013569:Synapses / Q000648:ultrastructure*
chemical_list: D000900:Anti-Bacterial Agents; D009355:Neomycin