Up-regulation of prestin mRNA expression in the organs of Corti of guinea pigs and rats following unilateral impulse noise exposure

Mazurek, Birgit; Haupt, H.; Amarjargal, Nyamaa; Yarin, Yury M.; Machulik, Astrid; Gross, Johann

doi:10.1016/j.heares.2007.05.008

Cited by 25 publications

(13 citation statements)

References 51 publications

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“…Our findings also demonstrate that OHC loss and dysfunction occurs concomitantly with upregulation in prestin levels in the lateral wall of surviving noise-exposed hair cells at all time points post-exposure. Consistent with this view, elevated prestin protein and gene expression in residual OHC has been reported in noise-exposed rodents and proposed as a compensatory mechanism by which hearing loss can be partially recovered after insult (Chen, 2006 ; Mazurek et al, 2007 ; Xia et al, 2013 ; Parham, 2015 ).…”

Section: Discussionmentioning

confidence: 57%

The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

et al. 2017

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Repeated noise exposure induces inflammation and cellular adaptations in the peripheral and central auditory system resulting in pathophysiology of hearing loss. In this study, we analyzed the mechanisms by which noise-induced inflammatory-related events in the cochlea activate glial-mediated cellular responses in the cochlear nucleus (CN), the first relay station of the auditory pathway. The auditory function, glial activation, modifications in gene expression and protein levels of inflammatory mediators and ultrastructural changes in glial-neuronal interactions were assessed in rats exposed to broadband noise (0.5–32 kHz, 118 dB SPL) for 4 h/day during 4 consecutive days to induce long-lasting hearing damage. Noise-exposed rats developed a permanent threshold shift which was associated with hair cell loss and reactive glia. Noise-induced microglial activation peaked in the cochlea between 1 and 10D post-lesion; their activation in the CN was more prolonged reaching maximum levels at 30D post-exposure. RT-PCR analyses of inflammatory-related genes expression in the cochlea demonstrated significant increases in the mRNA expression levels of pro- and anti-inflammatory cytokines, inducible nitric oxide synthase, intercellular adhesion molecule and tissue inhibitor of metalloproteinase-1 at 1 and 10D post-exposure. In noise-exposed cochleae, interleukin-1β (IL-1β), and tumor necrosis factor α (TNF-α) were upregulated by reactive microglia, fibrocytes, and neurons at all time points examined. In the CN, however, neurons were the sole source of these cytokines. These observations suggest that noise exposure causes peripheral and central inflammatory reactions in which TNF-α and IL-1β are implicated in regulating the initiation and progression of noise-induced hearing loss.

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Section: Discussionmentioning

confidence: 57%

The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

et al. 2017

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“…One group showed that rats exposed to long periods of noise had profound OHC loss and a nearly 5-fold increase in prestin mRNA after 5 days, followed by a return to the baseline by 4 weeks [37]. Other group also found 3 to 4 fold increase of prestin mRNA in the noise exposed cochleae [38]. Prestin protein and mRNA were investigated in the chronic salicylate administration induced hearing loss [39].…”

Section: Discussionmentioning

confidence: 99%

Prestin Regulation and Function in Residual Outer Hair Cells after Noise-Induced Hearing Loss

et al. 2013

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The outer hair cell (OHC) motor protein prestin is necessary for electromotility, which drives cochlear amplification and produces exquisitely sharp frequency tuning. TectaC1509G transgenic mice have hearing loss, and surprisingly have increased OHC prestin levels. We hypothesized, therefore, that prestin up-regulation may represent a generalized response to compensate for a state of hearing loss. In the present study, we sought to determine the effects of noise-induced hearing loss on prestin expression. After noise exposure, we performed cytocochleograms and observed OHC loss only in the basal region of the cochlea. Next, we patch clamped OHCs from the apical turn (9–12 kHz region), where no OHCs were lost, in noise-exposed and age-matched control mice. The non-linear capacitance was significantly higher in noise-exposed mice, consistent with higher functional prestin levels. We then measured prestin protein and mRNA levels in whole-cochlea specimens. Both Western blot and qPCR studies demonstrated increased prestin expression after noise exposure. Finally, we examined the effect of the prestin increase in vivo following noise damage. Immediately after noise exposure, ABR and DPOAE thresholds were elevated by 30–40 dB. While most of the temporary threshold shifts recovered within 3 days, there were additional improvements over the next month. However, DPOAE magnitudes, basilar membrane vibration, and CAP tuning curve measurements from the 9–12 kHz cochlear region demonstrated no differences between noise-exposed mice and control mice. Taken together, these data indicate that prestin is up-regulated by 32–58% in residual OHCs after noise exposure and that the prestin is functional. These findings are consistent with the notion that prestin increases in an attempt to partially compensate for reduced force production because of missing OHCs. However, in regions where there is no OHC loss, the cochlea is able to compensate for the excess prestin in order to maintain stable auditory thresholds and frequency discrimination.

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“…Because exposing animals to actual M16 firings is not practical in the laboratory, we began with simulated M16, obtaining the electrical waveform from a sound effects site and transducing it with several different types of amplifiers, speakers and exposure settings. Others [15-19] have also used computer simulations for impulse noise, for the same practical reasons. In the present study, the ability of furosemide to protect from exposure to actual M16 firing was also assessed.…”

Section: Discussionmentioning

confidence: 99%

Effects of furosemide on the hearing loss induced by impulse noise

Adelman

Weinberger

Kriksunov

et al. 2011

J Occup Med Toxicol

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BackgroundThe permanent hearing loss following exposure to intense noise can be due either to mechanical structural damage (tearing) caused directly by the noise or to metabolic (biochemical) damage resulting from the elevated levels of free radicals released during transduction of the sound overstimulation. Drugs which depress active cochlear mechanics (e.g. furosemide and salicylic acid) or anti-oxidants (which counteract the free radicals) are effective in reducing the threshold shift (TS) following broadband continuous noise. This study was designed to determine whether furosemide can reduce the TS following exposure to impulse noise, similar to its action with continuous broadband noise.MethodsShortly after furosemide injection, mice were exposed to simulated M16 rifle impulse noise produced by different loudspeakers and amplifiers in different exposure settings and, in other experiments, also to actual M16 rifle shots.ResultsDepending on the paradigm, the simulated noises either did not produce a TS, or the TS was reduced by furosemide. The drug was not effective in reducing TS resulting from actual impulse noise.ConclusionSimulated M16 rifle impulse noise may not truly replicate the rapid rise time and very high intensity of actual rifle shots so that the TS following exposure to such noise can be reduced by these drugs. On the other hand, actual M16 impulse noise probably causes direct (frank) mechanical damage, which is not reduced by these drugs.

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Up-regulation of prestin mRNA expression in the organs of Corti of guinea pigs and rats following unilateral impulse noise exposure

Cited by 25 publications

References 51 publications

The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

The Role of Glia in the Peripheral and Central Auditory System Following Noise Overexposure: Contribution of TNF-α and IL-1β to the Pathogenesis of Hearing Loss

Prestin Regulation and Function in Residual Outer Hair Cells after Noise-Induced Hearing Loss

Effects of furosemide on the hearing loss induced by impulse noise

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