Postnatal development, maturation and aging in the mouse cochlea and their effects on hair cell regeneration

Walters, Bradley J.; Zuo, Jian

doi:10.1016/j.heares.2012.11.009

Cited by 44 publications

(34 citation statements)

References 271 publications

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“…Mice are born with no hearing function (Ehret, 1976(Ehret, , 1985aWalters and Zuo, 2013), because their external ear has not yet formed and their middle ear is filled with a jelly-like material (Mikaelian and Ruben, 1965;Mikaelian, 1979). On the other hand, the cochleae of mice at birth are formed with an immature organ of Corti in which OHCs are differentiable from IHCs.…”

Section: Discussionmentioning

confidence: 99%

Noise-induced damage to ribbon synapses without permanent threshold shifts in neonatal mice

Shi¹,

Guo²,

Shen³

et al. 2015

Neuroscience

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Recently, ribbon synapses to the hair cells (HCs) in the cochlea have become a novel site of interest in the investigation of noise-induced cochlear lesions in adult rodents (Kujawa and Liberman, 2009; Lin et al., 2011; Liu et al., 2012; Shi et al., 2013). Permanent noise-induced damage to this type of synapse can result in subsequent degeneration of spiral ganglion neurons (SGNs) in the absence of permanent changes to hearing sensitivity. To verify whether noise exposure during an early developmental period produces a similar impact on ribbon synapses, the present study examined the damaging effects of noise exposure in neonatal Kunming mice. The animals received exposure to broadband noise at 105-decibel (dB) sound pressure level (SPL) for 2h on either postnatal day 10 (P10d) or postnatal day 14 (P14d), and then hearing function (based on the auditory brainstem response (ABR)) and cochlear morphology were evaluated during either postnatal weeks 3-4 (P4w) or postnatal weeks 7-8 (P8w). There were no significant differences in the hearing threshold between noise-exposed and control animals, which suggests that noise did not cause permanent loss of hearing sensitivity. However, noise exposure did produce a significant loss of ribbon synapses, particularly in P14d mice, which continued to increase from P4w to P8w. Additionally, a corresponding reduction in the amplitude of compound action potential (CAP) was observed in the noise-exposed groups at P4w and P8w, and the CAP latency was elongated, indicating a change in synaptic function.

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Section: Discussionmentioning

confidence: 99%

Noise-induced damage to ribbon synapses without permanent threshold shifts in neonatal mice

Shi¹,

Guo²,

Shen³

et al. 2015

Neuroscience

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“…Neural stem cells also decrease in number as the animal ages (Maslov et al, 2004), and this decrease in the stem cell reserve is implicated in the decline in tissue repair seen with aging (Jin et al, 2004). In the inner ear, a loss of competence to respond to multiple signaling pathways occurs as the cochlea matures (Walters and Zuo, 2013). As discussed above, this difference in responsiveness between the neonatal and adult cochlea is observed when overexpressing Atoh1, activating Wnt signaling, or manipulating Notch signaling and p27…”

Section: Cip1mentioning

confidence: 98%

“…3). Although our insights into the mechanisms responsible for such differences in responsiveness to gene manipulations in the neonatal and mature inner ear organs are limited, organs of these ages do display rather different gene expression profiles (reviewed by Walters and Zuo, 2013) and epigenetic differences, such as those at Sox2 enhancers (Waldhaus et al, 2012). In light of the important roles of epigenetic regulation in cellular senescence in other organs, one may postulate that epigenetic changes play a role in suppressing the expression of hair cell genes in supporting cells, possibly limiting the efficacy of reintroducing Atoh1.…”

Section: Kip1mentioning

confidence: 99%

Sensory hair cell development and regeneration: similarities and differences

et al. 2015

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Sensory hair cells are mechanoreceptors of the auditory and vestibular systems and are crucial for hearing and balance. In adult mammals, auditory hair cells are unable to regenerate, and damage to these cells results in permanent hearing loss. By contrast, hair cells in the chick cochlea and the zebrafish lateral line are able to regenerate, prompting studies into the signaling pathways, morphogen gradients and transcription factors that regulate hair cell development and regeneration in various species. Here, we review these findings and discuss how various signaling pathways and factors function to modulate sensory hair cell development and regeneration. By comparing and contrasting development and regeneration, we also highlight the utility and limitations of using defined developmental cues to drive mammalian hair cell regeneration.

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“…Finally, ectopic activation of the hair cell-specific transcription factor Atoh1 in supporting cells can drive their differentiation into hair cells [12, 22–24]. In all these cases, however, the capacity of mouse supporting cells to either divide or trans-differentiate into hair cells is lost between birth and the onset of hearing at two weeks of age [1, 9, 22, 23, 25]. …”

Section: Introductionmentioning

confidence: 99%

Transcriptomic Analysis of Mouse Cochlear Supporting Cell Maturation Reveals Large-Scale Changes in Notch Responsiveness Prior to the Onset of Hearing

Maass

Cai

et al. 2016

PLoS ONE

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Neonatal mouse cochlear supporting cells have a limited ability to divide and trans-differentiate into hair cells, but this ability declines rapidly in the two weeks after birth. This decline is concomitant with the morphological and functional maturation of the organ of Corti prior to the onset of hearing. However, despite this association between maturation and loss of regenerative potential, little is known of the molecular changes that underlie these events. To identify these changes, we used RNA-seq to generate transcriptional profiles of purified cochlear supporting cells from 1- and 6-day-old mice. We found many significant changes in gene expression during this period, many of which were related to regulation of proliferation, differentiation of inner ear components and the maturation of the organ of Corti prior to the onset of hearing. One example of a change in regenerative potential of supporting cells is their robust production of hair cells in response to a blockade of the Notch signaling pathway at the time of birth, but a complete lack of response to such blockade just a few days later. By comparing our supporting cell transcriptomes to those of supporting cells cultured in the presence of Notch pathway inhibitors, we show that the transcriptional response to Notch blockade disappears almost completely in the first postnatal week. Our results offer some of the first molecular insights into the failure of hair cell regeneration in the mammalian cochlea.

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Postnatal development, maturation and aging in the mouse cochlea and their effects on hair cell regeneration

Cited by 44 publications

References 271 publications

Noise-induced damage to ribbon synapses without permanent threshold shifts in neonatal mice

Noise-induced damage to ribbon synapses without permanent threshold shifts in neonatal mice

Sensory hair cell development and regeneration: similarities and differences

Transcriptomic Analysis of Mouse Cochlear Supporting Cell Maturation Reveals Large-Scale Changes in Notch Responsiveness Prior to the Onset of Hearing

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