Morphological changes in the cochlear nucleus of congenitally deaf white cats.
Investigations in animal models and humans have indicated that congenital deafness produces degenerative changes in the central auditory pathway. The cochlear nucleus is the first central structure that receives cochlear input, and may be considered the origin of ascending auditory pathways. In this context, we studied congenitally deaf white cats, who express early onset cochlear receptor loss, in order to assess the nature of structural changes in cells of the cochlear nucleus. It is conceivable that pathologic alterations in higher auditory structures are transneuronally distributed through this nucleus. The cochlear nuclei of nonwhite cats with normal hearing were compared to those of deaf white cats exhibiting hearing loss in excess of 70 dB SPL. The cochlear nuclei of the deaf white cats were smaller in volume by roughly 50%, with the ventral and dorsal divisions being equally affected. Cell body silhouette area was determined for spherical bushy cells of the anteroventral cochlear nucleus (AVCN), pyramidal cells of the dorsal cochlear nucleus (DCN), sensory neurons from the principal trigeminal nucleus, and motoneurons of the facial nucleus. We found no statistical difference in neuronal cell body size between nonauditory neurons of these two groups of cats, whereas auditory neurons of deaf white cats were 30.8-39.4% smaller than those of normal cats. These data imply that neuronal changes in congenitally deaf cats are specific to the auditory pathway. Although cochlear nucleus volume loss was uniform for both divisions, there was a differential effect on cell density: AVCN cell density increased by 40%, whereas DCN cell density was relatively unaffected (10% increase). Astrocyte density was also greater in the AVCN (52%) compared to that in the DCN (5%). These observations reveal a differential impact on cells in the cochlear nucleus to congenital deafness, suggesting selective processing impairment at this level. If similar patterns of degeneration occur in humans, such pathologies may underlie reduced processing of input from cochlear implants in congenitally deaf adults.
Saada
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AA
Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. saada@welchlink.welch.jhu.edu
Niparko
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JK
Ryugo
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DK
D000818:Animals; D001253:Astrocytes / Q000166:cytology / Q000473:pathology; D048588:Benzoxazines; D002371:Cat Diseases; D002415:Cats; D017626:Cochlear Nucleus / Q000166:cytology / Q000473:pathology*; D004396:Coloring Agents; D003638:Deafness / Q000235:genetics / Q000473:pathology / Q000662:veterinary*; D005154:Facial Nerve / Q000166:cytology / Q000473:pathology*; D009046:Motor Neurons / Q000166:cytology / Q000473:pathology; D009474:Neurons / Q000166:cytology / Q000473:pathology*; D009475:Neurons, Afferent / Q000166:cytology / Q000473:pathology; D010078:Oxazines; D017966:Pyramidal Cells / Q000166:cytology / Q000473:pathology; D012016:Reference Values; D014276:Trigeminal Nerve / Q000166:cytology / Q000473:pathology*
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