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Abstract
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.