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Publication : α-Synuclein deficiency and efferent nerve degeneration in the mouse cochlea: a possible cause of early-onset presbycusis.

First Author  Park SN Year  2011
Journal  Neurosci Res Volume  71
Issue  3 Pages  303-10
PubMed ID  21840348 Mgi Jnum  J:180897
Mgi Id  MGI:5308145 Doi  10.1016/j.neures.2011.07.1835
Citation  Park SN, et al. (2011) Alpha-synuclein deficiency and efferent nerve degeneration in the mouse cochlea: a possible cause of early-onset presbycusis. Neurosci Res 71(3):303-10
abstractText  OBJECTIVES/HYPOTHESIS: Efferent nerves under the outer hair cells (OHCs) play a role in the protection of these cells from loud stimuli. Previously, we showed that cochlear alpha-synuclein expression is localized to efferent auditory synapses at the base of the OHCs. To prove our hypothesis that alpha-synuclein deficiency and efferent auditory deficit might be a cause of hearing loss, we compared the morphology of efferent nerve endings and alpha-synuclein expression within the cochleae of two mouse models of presbycusis. STUDY DESIGN: Comparative animal study of presbycusis. METHODS: The C57BL/6J(C57) mouse strain, a well-known model of early-onset hearing loss, and the CBA mouse strain, a model of relatively late-onset hearing loss, were examined. Auditory brainstem responses and distortion product otoacoustic emissions were recorded, and cochlear morphology with efferent nerve ending was compared. Western blotting was used to examine alpha-synuclein expression in the cochlea. RESULTS: Compared with CBA mice, C57 mice showed earlier onset high-frequency hearing loss and decreased function in OHCs, especially within high-frequency regions. C57 mice demonstrated more severe pathologic changes within the cochlea, particularly within the basal turn, than CBA mice of the same age. Weaker alpha-synuclein and synaptophysin expression in the efferent nerve endings and cochlear homogenates in C57 mice was observed. CONCLUSIONS: Our results support the hypothesis that efferent nerve degeneration, possibly due to differential alpha-synuclein expression, is a potential cause of early-onset presbycusis. Further studies at the cellular level are necessary to verify our results.
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