Tinnitus pitch and minimum masking levels in different etiologies

Zagólski, Olaf; Stręk, Paweł

doi:10.3109/14992027.2014.893377

Cited by 10 publications

(5 citation statements)

References 46 publications

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“…We used 90dBSPL for 1h followed by 2h of silence, as we have previously shown to be able to generate tinnitus-like behavior without permanent threshold shifts [ 37 ]. Here, we show again that noise exposure at 9–11kHz does not cause altered GPIAS index at any particular frequency, similarly to studies of mice and guinea pigs [ 33 , 56 ], as well as for patients reporting noise exposure as tinnitus etiology [ 57 ]. Unfortunately, due to a low signal-to-noise ratio (SNR) of the GPIAS recordings, it was not possible to analyze responses to single trials, which would enable the investigation of tinnitus-like responses in individual animals.…”

Section: Discussionsupporting

confidence: 84%

Decreasing dorsal cochlear nucleus activity ameliorates noise-induced tinnitus perception in mice

et al. 2022

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Background The dorsal cochlear nucleus (DCN) is a region known to integrate somatosensory and auditory inputs and is identified as a potential key structure in the generation of phantom sound perception, especially noise-induced tinnitus. Yet, how altered homeostatic plasticity of the DCN induces and maintains the sensation of tinnitus is not clear. Here, we chemogenetically decrease activity of a subgroup of DCN neurons, Ca2+/Calmodulin kinase 2 α (CaMKII α)-positive DCN neurons, using Gi-coupled human M4 Designer Receptors Exclusively Activated by Designer Drugs (hM4Di DREADDs), to investigate their role in noise-induced tinnitus. Results Mice were exposed to loud noise (9–11kHz, 90dBSPL, 1h, followed by 2h of silence), and auditory brainstem responses (ABRs) and gap prepulse inhibition of acoustic startle (GPIAS) were recorded 2 days before and 2 weeks after noise exposure to identify animals with a significantly decreased inhibition of startle, indicating tinnitus but without permanent hearing loss. Neuronal activity of CaMKII α+ neurons expressing hM4Di in the DCN was lowered by administration of clozapine-N-oxide (CNO). We found that acutely decreasing firing rate of CaMKII α+ DCN units decrease tinnitus-like responses (p = 3e −3, n = 11 mice), compared to the control group that showed no improvement in GPIAS (control virus; CaMKII α-YFP + CNO, p = 0.696, n = 7 mice). Extracellular recordings confirmed CNO to decrease unit firing frequency of CaMKII α-hM4Di+ mice and alter best frequency and tuning width of response to sound. However, these effects were not seen if CNO had been previously administered during the noise exposure (n = 6 experimental and 6 control mice). Conclusion We found that lowering DCN activity in mice displaying tinnitus-related behavior reduces tinnitus, but lowering DCN activity during noise exposure does not prevent noise-induced tinnitus. Our results suggest that CaMKII α-positive cells in the DCN are not crucial for tinnitus induction but play a significant role in maintaining tinnitus perception in mice.

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Section: Discussionsupporting

confidence: 84%

Decreasing dorsal cochlear nucleus activity ameliorates noise-induced tinnitus perception in mice

et al. 2022

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“…We used 90dBSPL for 1h followed by 2h of silence, as we have previously shown to be able to generate tinnitus-like behavior without permanent threshold shifts (Winne et al, 2020). Here we show again that noise exposure at 9-11kHz frequency does not caused tinnitus-like behavior at a particular frequency, similarly to studies of mice and guinea pigs (Coomber et al, 2014; Longenecker and Galazyuk, 2016), as well as for patients reporting noise exposure as tinnitus etiology (Zagáolski and Strek, 2014).…”

Section: Discussionsupporting

confidence: 83%

Chemogenetically decreasing activity of the dorsal cochlear nucleus can ameliorate noise-induced tinnitus in mice

Malfatti

Ciralli

Hilscher³

et al. 2021

Preprint

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The dorsal cochlear nucleus (DCN) is a region known to integrate somatosensory and auditory inputs and is identified as a potential key structure in the generation of phantom sound perception, especially noise-induced tinnitus. Yet, how altered homeostatic plasticity of the DCN induces and maintains the sensation of tinnitus is not clear. Here, we chemogenetically decrease activity of a subgroup of DCN neurons, Ca2+/Calmodulin kinase 2α (CaMKIIα) positive DCN neurons, using Gi-coupled human M4 Designer Receptors Exclusively Activated by Designer Drugs (hM4Di DREADDs), to investigate their role in noise-induced tinnitus. Mice were over-exposed to loud noise (9-11kHz, 90dBSPL, 1h, followed by 2h of silence) and auditory brainstem responses (ABRs) and gap prepulse inhibition of acoustic startle (GPIAS) were recorded two days before and two weeks after noise exposure to identify animals with a significantly decreased inhibition of startle, indicating tinnitus but without permanent hearing loss. Neuronal activity of CaMKIIα+ neurons expressing hM4Di in the DCN was lowered by administration of clozapine-N-oxide (CNO). We found that acutely decreasing firing rate of CaMKIIα+ DCN units decrease tinnitus-like responses (p = 0.038, n = 11 mice), compared to the control group that showed no improvement in GPIAS (control virus; CaMKIIα-YFP + CNO, p = 0.696, n = 7 mice). Extracellular recordings confirmed CNO to decrease unit firing frequency of CaMKIIα-hM4Di+ mice and alter best frequency and tuning width of response to sound. However, these effects were not seen if CNO had been previously administered during the noise overexposure (n = 6 experimental and 6 control mice). Our results suggest that CaMKIIα-hM4Di positive cells in the DCN are not crucial for tinnitus induction but play a significant role in maintaining tinnitus perception in mice.

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“…The recognized methods are as follows: (1) Pitchmatching: Patients equate the pitch of an external pure-tone or narrow-band noise to that of the tinnitus [16]; (2) loudness matching: Patients equate the intensity of matching pure-tone or narrow-band noise to that of the tinnitus [17]; (3) minimum masking levels: Patients identify the minimum levels of broadband noise required to completely mask the perceived tinnitus [18]; and (4) residual inhibition: Patients report the intervals during which the tinnitus is partially or completely suppressed after external masking stimuli are removed. The primary reason for conducting psychoacoustic measurements of tinnitus is to quantify treatment outcomes and effectiveness [19].…”

Section: Discussionmentioning

confidence: 99%

Combination of gaps in noise detection and visual analog scale for measuring tinnitus components in patients treated with repetitive transcranial magnetic stimulation

Wang

et al. 2016

Auris Nasus Larynx

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Tinnitus pitch and minimum masking levels in different etiologies

Abstract: Tinnitus pitch and MML are etiology dependent.

Cited by 10 publications

References 46 publications

Decreasing dorsal cochlear nucleus activity ameliorates noise-induced tinnitus perception in mice

Decreasing dorsal cochlear nucleus activity ameliorates noise-induced tinnitus perception in mice

Chemogenetically decreasing activity of the dorsal cochlear nucleus can ameliorate noise-induced tinnitus in mice

Combination of gaps in noise detection and visual analog scale for measuring tinnitus components in patients treated with repetitive transcranial magnetic stimulation

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