Noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in mice

Shi, Lin; Liu, Ke; Wang, Haolin; Zhang, Yue; Hong, Zhijun; Wang, Mingyu; Wang, Xiaoyu; Jiang, Xuejun; Yang, Shiming

doi:10.3109/00016489.2015.1061699

Cited by 75 publications

(68 citation statements)

References 20 publications

(33 reference statements)

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“…Since the animals used in this study were 5 weeks of age upon surgery and 8 to 9 weeks of age upon euthanasia, the presence of sensorineural hearing loss is unlikely. Indeed, ABR thresholds of the mice in the current study are similar to thresholds of normal hearing C57Bl6 mice (Fujita et al, 2015, Shi et al, 2015). Moreover, VGLUT changes occurred only in the CN ipsilateral to the kanamycin injection, whereas sensorineural hearing loss would presumably affect both sides equally.…”

Section: Discussionsupporting

confidence: 73%

“…However, post-hoc tests were not significant for any of the tested frequencies (one-way ANOVA: p = 0.278, p = 0.128, p = 0.236, p = 0.241 for 12, 16, 20, and 30 kHz, respectively, corrected for multiple comparisons). ABR thresholds of age-matched control animals were similar to ABR thresholds of normal-hearing C57Bl6 mice (Fujita et al, 2015, Shi et al, 2015). …”

Section: Resultsmentioning

confidence: 53%

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Altered vesicular glutamate transporter distributions in the mouse cochlear nucleus following cochlear insult

et al. 2016

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Vesicular glutamate transporters 1 and 2 (VGLUT1 and VGLUT2) have distinct distributions in the cochlear nucleus that correspond to the sources of the labeled terminals. VGLUT1 is mainly associated with terminals of auditory nerve fibers, whereas VGLUT2 is mainly associated with glutamatergic terminals deriving from other sources that project to the cochlear nucleus (CN), including somatosensory and vestibular terminals. Previous studies in guinea pig have shown that cochlear damage results in a decrease of VGLUT1-labeled puncta and an increase in VGLUT2-labeled puncta. This indicates cross-modal compensation that is of potential importance in somatic tinnitus. To examine whether this effect is consistent across species and to provide a background for future studies, using transgenesis, the current study examines VGLUT expression profiles upon cochlear insult by intracochlear kanamycin injections in the mouse. Intracochlear kanamycin injections abolished ipsilateral ABR responses in all animals and reduced ipsilateral spiral ganglion neuron densities in animals that were sacrificed after four weeks, but not in animals that were sacrificed after three weeks. In all unilaterally deafened animals, VGLUT1 density was decreased in CN regions that receive auditory nerve fiber terminals, i.e. in the deep layer of the dorsal cochlear nucleus (DCN), in the interstitial region where the auditory nerve enters the CN, and in the magnocellular region of the antero- and posteroventral CN. In contrast, density of VGLUT2 expression was upregulated in the fusiform cell layer of the DCN and in the granule cell lamina, which are known to receive somatosensory and vestibular terminals. These results show that a cochlear insult induces cross-modal compensation in the cochlear nucleus of the mouse, confirming previous findings in guinea pig, and that these changes are not dependent on the occurrence of spiral ganglion neuron degeneration.

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Section: Discussionsupporting

confidence: 73%

Section: Resultsmentioning

confidence: 53%

Altered vesicular glutamate transporter distributions in the mouse cochlear nucleus following cochlear insult

et al. 2016

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“…In our laboratories, the synaptopathy has been largely permanent, indeed progressive, in multiple species. There are reports, however, that spontaneous re-innervation can be seen (Puel et al, 1995; Pujol and Puel, 1999; Sun et al, 2001), or that some of the immediate synapse loss may be reversible (Liu et al, 2012; Shi et al, 2013, 2015, 2016; Song et al, 2016). The source(s) of these discrepancies remain to be identified.…”

Section: Discussionmentioning

confidence: 99%

Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms

2017

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Common causes of hearing loss in humans - exposure to loud noise or ototoxic drugs and aging - often damage sensory hair cells, reflected as elevated thresholds on the clinical audiogram. Recent studies in animal models suggest, however, that well before this overt hearing loss can be seen, a more insidious, but likely more common, process is taking place that permanently interrupts synaptic communication between sensory inner hair cells and subsets of cochlear nerve fibers. The silencing of affected neurons alters auditory information processing, whether accompanied by threshold elevations or not, and is a likely contributor to a variety of perceptual abnormalities, including speech-in-noise difficulties, tinnitus and hyperacusis. Work described here will review structural and functional manifestations of this cochlear synaptopathy and will consider possible mechanisms underlying its appearance and progression in ears with and without traditional ‘hearing loss’ arising from several common causes in humans.

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“…In addition, the recent surge of interest in hidden hearing loss and Bsynaptopathy^has heightened interest in TTS as a risk factor for primary neural loss. This phenomenon appears robust in CBA/CaJ (Kujawa and Liberman 2006, 2009) and FVB/nJ mice (Paquette et al 2016) but potentially less so in B6 (Shi et al 2015). What may distinguish mouse strains and species in the severity of synaptopathy from a single exposure is the extent of synaptic repair Song et al 2016).…”

Section: The Meaning and Significance Of Ttsmentioning

confidence: 99%

Application of Mouse Models to Research in Hearing and Balance

Ohlemiller

Jones

Johnson

2016

JARO

103

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Laboratory mice (Mus musculus) have become the major model species for inner ear research. The major uses of mice include gene discovery, characterization, and confirmation. Every application of mice is founded on assumptions about what mice represent and how the information gained may be generalized. A host of successes support the continued use of mice to understand hearing and balance. Depending on the research question, however, some mouse models and research designs will be more appropriate than others. Here, we recount some of the history and successes of the use of mice in hearing and vestibular studies and offer guidelines to those considering how to apply mouse models.

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Noise induced reversible changes of cochlear ribbon synapses contribute to temporary hearing loss in mice

Cited by 75 publications

References 20 publications

Altered vesicular glutamate transporter distributions in the mouse cochlear nucleus following cochlear insult

Altered vesicular glutamate transporter distributions in the mouse cochlear nucleus following cochlear insult

Cochlear synaptopathy in acquired sensorineural hearing loss: Manifestations and mechanisms

Application of Mouse Models to Research in Hearing and Balance

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