Abstract:Inhibition of cochlear amplifier gain by the medial olivocochlear (MOC) efferent system has several putative roles: aiding listening in noise, protection against damage from acoustic overexposure, and slowing age-induced hearing loss. The human MOC reflex has been studied almost exclusively by measuring changes in otoacoustic emissions. However, to help understand how the MOC system influences what we hear, it is important to have measurements of the MOC effect on the total output of the organ of Corti, i.e., … Show more
“…To directly compare the functional effects of each type of inhibition, it would be necessary to derive a level series function and quantify MOC reflex inhibition in terms of “effective attenuation” (i.e., the amount of stimulus gain in dB needed to overcome the effects of inhibition; see Puria et al, 1996; Lichtenhan et al, 2016, and Smith et al, 2017). Because one presentation level was used in this study, we cannot calculate effective attenuation from our data.…”
Section: Discussionmentioning
confidence: 99%
“…Experiments in laboratory animals are also planned to identify the spatial origin(s) of OAE and FFR distortion product components, and elucidate the hypothesized relationship between pre-neural and neural distortion. For example, slow injection of cell-specific ototoxic pharmaceuticals into the cochlear apex can be used to sequentially manipulate finely spaced cochlear regions, and the time course of distortion product component ablation can identify the region of origination (Lichtenhan et al, 2016). This technique overcomes limitations associated with passive diffusion of ototoxic agents (e.g., limited treatment of the high-frequency, basal half of the cochlear spiral), which is imperative for studying distortion products in OAEs and FFRs from low-frequency stimuli.…”
Section: Discussionmentioning
confidence: 99%
“…However, a major limitation of this approach is that OAEs are insensitive to MOC reflex effects on the neural ensembles that mediate human hearing, and the functional consequences of this mechanism remain unclear. To directly assess the degree to which efferent-induced changes in inner ear mechanics are maintained beyond the cochlea, it is necessary to understand relationships between pre-neural and neural measurements of the MOC reflex (Lichtenhan et al, 2016; Smith et al, 2017). …”
Distortion product otoacoustic emissions (DPOAEs) and distortion product frequency following responses (DPFFRs) are respectively pre-neural and neural measurements associated with cochlear nonlinearity. Because cochlear nonlinearity is putatively linked to outer hair cell electromotility, DPOAEs and DPFFRs may provide complementary measurements of the human medial olivocochlear (MOC) reflex, which directly modulates outer hair cell function. In this study, we first quantified MOC reflex-induced DPOAE inhibition at spectral fine structure peaks in 22 young human adults with normal hearing. The f1 and f2 tone pairs producing the largest DPOAE fine structure peak for each subject were then used to evoke DPFFRs with and without MOC reflex activation to provide a related neural measure of efferent inhibition. We observed significant positive relationships between DPOAE fine structure peak inhibition and inhibition of DPFFR components representing neural phase locking to f2 and 2f1-f2, but not f1. These findings may support previous observations that the MOC reflex inhibits DPOAE sources differentially. That these effects are maintained and represented in the auditory brainstem suggests that the MOC reflex may exert a potent influence on subsequent subcortical neural representation of sound.
“…To directly compare the functional effects of each type of inhibition, it would be necessary to derive a level series function and quantify MOC reflex inhibition in terms of “effective attenuation” (i.e., the amount of stimulus gain in dB needed to overcome the effects of inhibition; see Puria et al, 1996; Lichtenhan et al, 2016, and Smith et al, 2017). Because one presentation level was used in this study, we cannot calculate effective attenuation from our data.…”
Section: Discussionmentioning
confidence: 99%
“…Experiments in laboratory animals are also planned to identify the spatial origin(s) of OAE and FFR distortion product components, and elucidate the hypothesized relationship between pre-neural and neural distortion. For example, slow injection of cell-specific ototoxic pharmaceuticals into the cochlear apex can be used to sequentially manipulate finely spaced cochlear regions, and the time course of distortion product component ablation can identify the region of origination (Lichtenhan et al, 2016). This technique overcomes limitations associated with passive diffusion of ototoxic agents (e.g., limited treatment of the high-frequency, basal half of the cochlear spiral), which is imperative for studying distortion products in OAEs and FFRs from low-frequency stimuli.…”
Section: Discussionmentioning
confidence: 99%
“…However, a major limitation of this approach is that OAEs are insensitive to MOC reflex effects on the neural ensembles that mediate human hearing, and the functional consequences of this mechanism remain unclear. To directly assess the degree to which efferent-induced changes in inner ear mechanics are maintained beyond the cochlea, it is necessary to understand relationships between pre-neural and neural measurements of the MOC reflex (Lichtenhan et al, 2016; Smith et al, 2017). …”
Distortion product otoacoustic emissions (DPOAEs) and distortion product frequency following responses (DPFFRs) are respectively pre-neural and neural measurements associated with cochlear nonlinearity. Because cochlear nonlinearity is putatively linked to outer hair cell electromotility, DPOAEs and DPFFRs may provide complementary measurements of the human medial olivocochlear (MOC) reflex, which directly modulates outer hair cell function. In this study, we first quantified MOC reflex-induced DPOAE inhibition at spectral fine structure peaks in 22 young human adults with normal hearing. The f1 and f2 tone pairs producing the largest DPOAE fine structure peak for each subject were then used to evoke DPFFRs with and without MOC reflex activation to provide a related neural measure of efferent inhibition. We observed significant positive relationships between DPOAE fine structure peak inhibition and inhibition of DPFFR components representing neural phase locking to f2 and 2f1-f2, but not f1. These findings may support previous observations that the MOC reflex inhibits DPOAE sources differentially. That these effects are maintained and represented in the auditory brainstem suggests that the MOC reflex may exert a potent influence on subsequent subcortical neural representation of sound.
“…It is possible that the pressure against the TM, as well as the mass of the gel-soaked electrode tip, caused the threshold shifts. TM electrodes likely do not cause a shift in hearing sensitivity when using free field stimuli because expandable foam insert earphones are not used and thus there is less medial pressure imparted on the electrode (e.g., Lichtenhan et al 2015). Pure tone threshold data was solely collected by the first author.…”
Section: Discussionmentioning
confidence: 99%
“…TM electrodes provide superior signal-to-noise ratios compared to other extra-tympanic electrodes and are a non-invasive alternative to using trans-tympanic electrodes, which require a tympanotomy. Electrocochleography with a TM electrode has been used for a wide variety of clinical (e.g., Ferraro 2010) and basic investigation purposes (e.g., Chertoff et al 2010; Lichtenhan & Chertoff 2008; Lichtenhan et al 2015); however, no experiment has investigated the effects of TM electrode placement and contact location on behavioral hearing thresholds.…”
Objective
To determine if tympanic membrane (TM) electrodes induce behavioral pure tone threshold shifts.
Design
Pure tone thresholds (250–8000 Hz) were measured twice in test (n=18) and control (n=10) groups. TM electrodes were placed between first and second threshold measurements in the test group, whereas the control group did not receive electrodes. Pure tone threshold shifts were compared between groups. The effect of TM electrode contact location on threshold shifts was evaluated in the test group.
Results
TM electrodes significantly increased average low-frequency thresholds, 7.5 dB at 250 Hz and 4.2 dB at 500 Hz, and shifts were as large as 25 dB in individual ears. Also, threshold shifts did not appear to vary at any frequency with TM electrode contact location.
Conclusions
Low-frequency threshold shifts occur when using TM electrodes and insert earphones. These findings are relevant to interpreting electrocochleographic responses to low-frequency stimuli.
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