Prolonged noise exposure-induced auditory threshold shifts in rats

Chen, Guang-Di; Decker, Brandon; Muthaiah, Vijaya Prakash Krishnan; Sheppard, Adam; Salvi, Richard

doi:10.1016/j.heares.2014.08.004

Cited by 44 publications

(32 citation statements)

References 53 publications

(88 reference statements)

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“…The rationale for using these two exposures is that they are identical to those being used in ongoing behavioral studies designed to obtain behavioral measures of hearing loss, hyperacusis and tinnitus. The advantage of using long-duration exposures is that all animals develop the similar asymptotic threshold shift after they have been in the noise for >24 h (Carder and Miller, 1972, Salvi et al, 1978, Chen et al, 2014a). These long-duration exposures reduce between subject variability in the amount of hearing loss and cochlear pathology compared to intense, short duration (e.g., 1–3 h) exposures.…”

Section: Methodsmentioning

confidence: 99%

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

2016

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The effects of intense noise exposure on the classical auditory pathway have been extensively investigated; however, little is known about the effects of noise-induced hearing loss on non-classical auditory areas in the brain such as the lateral amygdala (LA) and striatum (Str). To address this issue, we compared the noise-induced changes in spontaneous and tone-evoked responses from multiunit clusters (MUC) in the LA and Str with those seen in auditory cortex (AC). High-frequency octave band noise (10–20 kHz) and narrow band noise (16–20 kHz) induced permanent thresho ld shifts (PTS) at high-frequencies within and above the noise band but not at low frequencies. While the noise trauma significantly elevated spontaneous discharge rate (SR) in the AC, SRs in the LA and Str were only slightly increased across all frequencies. The high-frequency noise trauma affected tone-evoked firing rates in frequency and time dependent manner and the changes appeared to be related to severity of noise trauma. In the LA, tone-evoked firing rates were reduced at the high-frequencies (trauma area) whereas firing rates were enhanced at the low-frequencies or at the edge-frequency dependent on severity of hearing loss at the high frequencies. The firing rate temporal profile changed from a broad plateau to one sharp, delayed peak. In the AC, tone-evoked firing rates were depressed at high frequencies and enhanced at the low frequencies while the firing rate temporal profiles became substantially broader. In contrast, firing rates in the Str were generally decreased and firing rate temporal profiles become more phasic and less prolonged. The altered firing rate and pattern at low frequencies induced by high frequency hearing loss could have perceptual consequences. The tone-evoked hyperactivity in low-frequency MUC could manifest as hyperacusis whereas the discharge pattern changes could affect temporal resolution and integration.

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Section: Methodsmentioning

confidence: 99%

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

2016

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“…To ensure that the noise exposure caused significant hearing loss in the left (exposed) ear, but not the right (plugged) ear, the speaker was positioned 20 cm directly in front of the left ear, and the opposite ear was occluded with an ear plug; hearing sensitivity in the right ear was estimated by reversing the left-right conditions (Note: the maximal interaural sound attenuation obtained with ear plugging is approximately 40 dB). Stimuli were synthesized and generated by Tucker-Davis Technologies (TDT) hardware and software (BioSigRP) and delivered to a loudspeaker (FT28D, Fostex) as previously described, (Chen et al, 2014). Biological signals from the electrodes were routed to a TDT Headstage-4 amplifier (5020X) and filtered from 100-3000 Hz.…”

Section: Methodsmentioning

confidence: 99%

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Manohar

Dahar

Adler

et al. 2016

Molecular and Cellular Neuroscience

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Severe noise-induced damage to the inner ear leads to auditory nerve fiber degeneration thereby reducing the neural input to the cochlear nucleus (CN). Paradoxically, this leads to a significant increase in spontaneous activity in the CN which has been linked to tinnitus, hyperacusis and ear pain. The biological mechanisms that lead to an increased spontaneous activity are largely unknown, but could arise from changes in glutamatergic or GABAergic neurotransmission or neuroinflammation. To test this hypothesis, we unilaterally exposed rats for 2 h to a 126 dB SPL narrow band noise centered at 12 kHz. Hearing loss measured by auditory brainstem responses exceeded 55 dB from 6 to 32 kHz. The mRNA from the exposed CN was harvested at 14 or 28 days post-exposure and qRT-PCR analysis was performed on 168 genes involved in neural inflammation, neuropathic pain and glutamatergic or GABAergic neurotransmission. Expression levels of mRNA of Slc17a6 and Gabrg3, involved in excitation and inhibition respectively, were significantly increased at 28 days post-exposure, suggesting a possible role in the CN spontaneous hyperactivity associated with tinnitus and hyperacusis. In the pain and inflammatory array, noise exposure up-regulated mRNA expression levels of four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 and Ntrk1 and decreased mRNA expression levels of two more genes, Ccl12 and Il1β. Pain/inflammatory gene expression changes via Ntrk1 signaling may induce sterile inflammation, neuropathic pain, microglial activation and migration of nerve fibers from the trigeminal nerve and cuneate and vestibular nuclei into the CN. These changes could contribute to somatic tinnitus, hyperacusis and otalgia.

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“…Details of the noise exposure can be found in our previous study (Chen et al, 2014b). Briefly, the six rats were housed individually in their home cages in the Lab Animal Facility and exposed to a 102 dB SPL (+/− 2.5 dB), 16–20 kHz noise 24 h per day for 4 weeks.…”

Section: Methodsmentioning

confidence: 99%

“…Our auditory brainstem response (ABR) procedures are described in detail in our earlier publications (Chen et al, 2014b; Chen et al, 2010; Kane et al, 2012). Rats were anesthetized with a ketamine (50 mg/kg)/xylazine (6 mg/kg) cocktail (i.p.)…”

Section: Methodsmentioning

confidence: 99%

Noise-induced hearing loss induces loudness intolerance in a rat Active Sound Avoidance Paradigm (ASAP)

et al. 2017

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Hyperacusis is a loudness hypersensitivity disorder in which moderate-intensity sounds are perceived as extremely loud, aversive and/or painful. To assess the aversive nature of sounds, we developed an Active Sound Avoidance Paradigm (ASAP) in which rats altered their place preference in a Light/Dark shuttle box in response to sound. When no sound (NS) was present, rats spent more than 95% of the time in the Dark Box versus the transparent Light Box. However, when a 60 or 90 dB SPL noise (2–20 kHz, 2–8 kHz, or 16–20 kHz bandwidth) was presented in the Dark Box, the rats’ preference for the Dark Box significantly decreased. Percent time in the dark decreased as sound intensity in the Dark Box increased from 60 dB to 90 dB SPL. Interestingly, the magnitude of the decrease was not a monotonic function of intensity for the 16–20 kHz noise and not related to the bandwidth of the 2–20 kHz and 2–8 kHz noise bands, suggesting that sound avoidance is not solely dependent on loudness but the aversive quality of the noise as well. Afterwards, we exposed the rats for 28 days to a 16–20 kHz noise at 102 dB SPL; this exposure produced a 30–40 dB permanent threshold shift at 16 and 32 kHz. Following the noise exposure, the rats were then retested on the ASAP paradigm. High-frequency hearing loss did not alter Dark Box preference in the no-sound condition. However, when the 2–20 kHz or 2–8 kHz noise was presented at 60 or 90 dB SPL, the rats avoided the Dark Box significantly more than they did before the exposure, indicating these two noise bands with energy below the region of hearing loss were perceived as more aversive. In contrast, when the 16–20 kHz noise was presented at 60 or 90 dB SPL, the rats remained in the Dark Box presumably because the high-frequency hearing loss made 16–20 kHz noise less audible and less aversive. These results indicate that when rats develop a high-frequency hearing loss, they become less tolerant of low frequency noise, i.e., high intensity sounds are perceived as more aversive and should be avoided.

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Prolonged noise exposure-induced auditory threshold shifts in rats

Cited by 44 publications

References 53 publications

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

Noise trauma induced plastic changes in brain regions outside the classical auditory pathway

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Noise-induced hearing loss induces loudness intolerance in a rat Active Sound Avoidance Paradigm (ASAP)

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