SYNAPTIC LOSS IN THE CENTRAL NUCLEUS OF THE INFERIOR COLLICULUS CORRELATES WITH SENSORINEURAL HEARING-LOSS IN THE C57BL 6 MOUSE MODEL OF PRESBYCUSIS/

Citation
Am. Kazee et al., SYNAPTIC LOSS IN THE CENTRAL NUCLEUS OF THE INFERIOR COLLICULUS CORRELATES WITH SENSORINEURAL HEARING-LOSS IN THE C57BL 6 MOUSE MODEL OF PRESBYCUSIS/, Hearing research, 89(1-2), 1995, pp. 109-120
Citations number
46
Categorie Soggetti
Neurosciences,Acoustics
Journal title
ISSN journal
03785955
Volume
89
Issue
1-2
Year of publication
1995
Pages
109 - 120
Database
ISI
SICI code
0378-5955(1995)89:1-2<109:SLITCN>2.0.ZU;2-G
Abstract
Between 3 and 25 months of age, light and electron microscopic feature s of principal neurons in the central nucleus of the inferior collicul us of the C57BL/6 mouse were quantitated. This mouse strain has a gene tic defect producing progressive sensorineural hearing loss which star ts during young adulthood (2 months of age) with high-frequency sounds . During the second year of life, hearing is severely impaired, progre ssively involving all frequencies. The hearing loss was documented in the present study by auditory brainstem recordings of the mice at vari ous ages. The cochleas from many of the same animals showed massive lo ss of both inner and outer hair cells beginning at the base (high-freq uency region) and progressing with age along the entire length to the apex (low-frequency region). In the inferior colliculi, there was a si gnificant decrease in the size of principal neurons in the central nuc leus. There was a dramatic decrease in the number of synapses of all m orphologic types on principal neuronal somas. The percentage of somati c membrane covered by synapses decreased by 67%, A ventral (high frequ ency) 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 no ted in the central nucleus of the inferior colliculus, in which respon se properties of neurons normally sensitive to high-frequency sounds b ecome more sensitive to low-frequency sounds. The synaptic loss noted in this study may be due to more than the loss of primary afferent pat hways. It may represent alterations of the complex synaptic circuitry related to the central deficits of presbycusis.