| First Author | Kazee AM | Year | 1995 |
| Journal | Hear Res | Volume | 89 |
| Issue | 1-2 | Pages | 109-20 |
| PubMed ID | 8600115 | Mgi Jnum | J:30601 |
| Mgi Id | MGI:78100 | Doi | 10.1016/0378-5955(95)00128-6 |
| Citation | Kazee AM, et al. (1995) Synaptic loss in the central nucleus of the inferior colliculus correlates with sensorineural hearing loss in the C57BL/6 mouse model of presbycusis. Hear Res 89(1-2):109-20 |
| abstractText | Between 3 and 25 months of age, light and electron microscopic features of principal neurons in the central nucleus of the inferior colliculus of the C57BL/6 mouse were quantitated. This mouse strain has a genetic defect producing progressive sensorineural hearing loss which starts during young adulthood (2 months of age) with high-frequency sounds. During the second year of life, hearing is severely impaired, progressively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at various ages. The cochleas from many of the same animals showed massive loss of both inner and outer hair cells beginning at the base (high-frequency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a significant decrease in the size of principal neurons in the central nucleus. There was a dramatic decrease in the number of synapses of all morphologic types on principal neuronal somas. The percentage of somatic membrane covered by synapses decreased by 67%. A ventral (high frequency) to dorsal (low frequency) gradient of synaptic loss could not be identified within the central nucleus. These synaptic changes may be related to the equally dramatic physiologic changes which have been noted in the central nucleus of the inferior colliculus, in which response properties of neurons normally sensitive to high-frequency sounds become more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pathways. It may represent alterations of the complex synaptic circuitry related to the central deficits of presbycusis. |
