acoustic distortion Search Results


fat-mimicking acoustic distortion layers  (CIRS Inc)
90
CIRS Inc fat-mimicking acoustic distortion layers
Fat Mimicking Acoustic Distortion Layers, supplied by CIRS Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/fat+mimicking+acoustic+distortion+layers/pmc07592964-67-0-37
Average 90 stars, based on 1 article reviews
fat-mimicking acoustic distortion layers - by Bioz Stars, 2026-09
90/100 stars
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tympanometry with acoustic stapedius reflex (asr) and distortion product otoacoustic emission (dpoae) titan  (Interacoustics AS)
90
Interacoustics AS tympanometry with acoustic stapedius reflex (asr) and distortion product otoacoustic emission (dpoae) titan
Tympanometry With Acoustic Stapedius Reflex (Asr) And Distortion Product Otoacoustic Emission (Dpoae) Titan, supplied by Interacoustics AS, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/tympanometry+with+acoustic+stapedius+reflex++asr++and+distortion+product+otoacoustic+emission++dpoae++titan/pmc09387814-117-12-25
Average 90 stars, based on 1 article reviews
tympanometry with acoustic stapedius reflex (asr) and distortion product otoacoustic emission (dpoae) titan - by Bioz Stars, 2026-09
90/100 stars
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distortion product otoacoustic emission ( dpoae)  (Industrial Acoustics Co Inc)
90
Industrial Acoustics Co Inc distortion product otoacoustic emission ( dpoae)
Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in <t>distortion-product</t> <t>otoacoustic</t> emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.
Distortion Product Otoacoustic Emission ( Dpoae), supplied by Industrial Acoustics Co Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/distortion+product+otoacoustic+emission+++dpoae+/pmc08914323-363-10-32
Average 90 stars, based on 1 article reviews
distortion product otoacoustic emission ( dpoae) - by Bioz Stars, 2026-09
90/100 stars
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acoustic distortion  (EcoDesign Inc)
90
EcoDesign Inc acoustic distortion
Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in <t>distortion-product</t> <t>otoacoustic</t> emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.
Acoustic Distortion, supplied by EcoDesign Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/acoustic+distortion/10__1109_slash_access__2018__2886018-115-0-9
Average 90 stars, based on 1 article reviews
acoustic distortion - by Bioz Stars, 2026-09
90/100 stars
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distortion product acoustic emissions, dpoaes with the interacoustics titan system  (Interacoustics AS)
90
Interacoustics AS distortion product acoustic emissions, dpoaes with the interacoustics titan system
Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in <t>distortion-product</t> <t>otoacoustic</t> emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.
Distortion Product Acoustic Emissions, Dpoaes With The Interacoustics Titan System, supplied by Interacoustics AS, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/distortion+product+acoustic+emissions++dpoaes+with+the+interacoustics+titan+system/pm33225761-203-15-14
Average 90 stars, based on 1 article reviews
distortion product acoustic emissions, dpoaes with the interacoustics titan system - by Bioz Stars, 2026-09
90/100 stars
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acoustic distortion  (Myspace LLC)
90
Myspace LLC acoustic distortion
Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in <t>distortion-product</t> <t>otoacoustic</t> emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.
Acoustic Distortion, supplied by Myspace LLC, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/acoustic+distortion/10__1109_slash_tcomm__2018__2889331-327-0-0
Average 90 stars, based on 1 article reviews
acoustic distortion - by Bioz Stars, 2026-09
90/100 stars
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acoustic mesh distortion  (Abaqus Inc)
86
Abaqus Inc acoustic mesh distortion
Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in <t>distortion-product</t> <t>otoacoustic</t> emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.
Acoustic Mesh Distortion, supplied by Abaqus Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/acoustic+distortion/acoustic+distortion+mesh/10__1016_slash_j__ijimpeng__2024__104999-226-4-13
Average 86 stars, based on 1 article reviews
acoustic mesh distortion - by Bioz Stars, 2026-09
86/100 stars
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Image Search Results


Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in distortion-product otoacoustic emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.

Journal: iScience

Article Title: Loss of central mineralocorticoid or glucocorticoid receptors impacts auditory nerve processing in the cochlea

doi: 10.1016/j.isci.2022.103981

Figure Lengend Snippet: Improved suprathreshold hearing function in MRGR cKO (A) Workflow of the experiment. 8 weeks after birth, adult, developed mice were checked for hearing function and injected with tamoxifen (TMX). After 4 weeks of recovery, the hearing was measured again and mice were sacrificed to collect brain and cochlea tissue. The TMX induction led to a tissue-specific deletion of MR and GR under the promoter of CaMKIIα, which is expressed in the forebrain, but not the cochlea. (B) No difference between thresholds in MRGR cKO and control mice with click- (unpaired Student’s t test, t(50) = 0.620, p = 0.538, WT: n = 12/24, KO: n = 14/28 mice/ears), noise-burst evoked auditory brainstem responses ( ABR ; t(50) = 0.451, p = 0.653, WT: n = 12/24, KO: n = 14/28 mice/ears), as well as pure tone ABR (two-way ANOVA, F(1,8) = 0.191, p = 0.663, WT: n = 10, KO: n = 11 mice/ears). (C) No difference between thresholds in MRGR cKO and control mice in distortion-product otoacoustic emission ( DPOAE ) thresholds (two-way ANOVA, F(1,5) = 1.772, p = 0.186, WT: n = 5/10, KO: n = 8/16 mice/ears). (D) No difference between CAP thresholds (two-way ANOVA, F(1,16) = 0.368, p = 0.5443, WT: n = 5/9, KO: n = 7/13 mice/ears) between MRGR cKO and control mice. (E) Schematic drawing of the auditory pathway and correlated ABR waves. (F) Left panel: Increased ABR wave I amplitude in MRGR cKO (two-way ANOVA, F(1,17) = 10.80, p = 0.0011, WT: n = 12/24, KO: n = 15/30 mice/ears) and (right panel) increased ABR wave IV amplitude (two-way ANOVA, F(1,17) = 31.62, p < 0.0001, WT: n = 12/24, KO: n = 14/28 mice/ears) compared to controls. (G) Shortened CAP latency of wave I in MRGR cKO mice (two-way ANOVA, F(1,620) = 70.94, p = 0.0022, WT: n = 6/11, KO: n = 7/13 mice/ears) as compared to controls. (H) Larger modulation depth function in MRGR cKO mice (two-way ANOVA, F(1,572) = 11.38, p = 0.0008, WT: n = 19, KO: n = 18 mice/ears). (I) Increased growth function in MRGR cKO mice (two-way ANOVA, F(1,688) = 5.210, p = 0.023, WT: n = 18, KO: n = 20 mice/ears) compared to controls. (J) Increased modulation transfer function in MRGR cKO mice (two-way ANOVA, F(1,473) = 14.37, p = 0.0002, n = 19 mice/ears) compared to WT mice. Mean ± SEM. ∗ = p < 0.05, ∗∗ = p < 0.01, ∗∗∗ = p < 0.001, n.s. = not significant (p > 0.05). AN = auditory nerve, CN = cochlear nucleus, SOC = superior olivary complex, IC = inferior colliculus, MGB = medial geniculate body, AC = auditory cortex.

Article Snippet: Hearing function was studied before and after TMX-induction by measuring Distortion Product Otoacoustic Emission ( DPOAE ), Auditory Brainstem Responses ( ABR ) and Elelctrocochleographic Recordings in a soundproof chamber (IAC 400-A, Industrial Acoustics Company GmbH, Niederkrüchten).

Techniques: Injection, Control