Dataset Information

Histology of the Cochlear Outer Sulcus Cells in Normal Human Ears, Presbycusis, and Meniere's Disease.

ABSTRACT:

Hypothesis

Outer sulcus cell features and distribution are hypothesized to differ throughout regions of the human cochlea and between diseased and normal specimens.

Background

Outer sulcus cells play a role in inner ear fluid homeostasis. However, their anatomy and distribution in the human are not well described.

Methods

Temporal bone specimens with normal hearing (n = 10), Menière's disease (n = 10), presbycusis with flat audiograms (n = 4), and presbycusis with sloping audiograms (n = 5) were examined by light microscopy. Outer sulcus cells were assessed quantitatively and qualitatively in each cochlear turn. One specimen was stained for tubulin immunofluorescence and imaged using confocal microscopy.

Results

Outer sulcus cells interface with endolymph throughout the cochlea, with greatest contact in the apical turn. Mean outer sulcus cell counts in the upper apical turn (8.82) were generally smaller (all p < 0.05) than those of the upper basal (17.71), lower middle (18.99) upper middle (18.23), and lower apical (16.42) turns. Mean outer sulcus cell counts were higher (p < 0.05) in normal controls (20.1) than in diseased specimens (15.29). There was a significant correlation between mean cell counts and tonotopically expected hearing thresholds in the upper basal (r = -0.662, p = 0.0001), lower middle (r = -0.565, p = 0.0017), and upper middle (r = -0.507, p = 0.0136) regions. Other differences in cell morphology, distribution, or relationship with Claudius cells were not appreciated between normal and diseased specimens. Menière's specimens had no apparent unique features in the cochlear apex. Immunofluorescence staining demonstrated outer sulcus cells extending into the spiral ligament in bundles forming tapering processes which differed between the cochlear turns in morphology.

Conclusion

Outer sulcus cells vary throughout the cochlear turns and correlate with hearing status, but not in a manner specific to the underlying diagnoses of Menière's disease or presbycusis.

SUBMITTER: Christov F

PROVIDER: S-EPMC7275934 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:ObjectivesTo determine whether suprathreshold measures of auditory function, such as distortion-product otoacoustic emissions (DPOAEs) and auditory brainstem responses (ABRs), are correlated with noise exposure history in normal-hearing human ears. Recent data from animal studies have revealed significant deafferentation of auditory nerve fibers after full recovery from temporary noise-induced hearing loss. Furthermore, these data report smaller ABR wave I amplitudes in noise-exposed animal ears when compared with non-noise-exposed control animals or prenoise exposure amplitudes in the same animal. It is unknown whether a similar phenomenon exists in the normal-hearing, noise-exposed human ear.DesignThirty normal-hearing human subjects with a range of noise exposure backgrounds (NEBs) participated in this study. NEB was quantified by the use of a noise exposure questionnaire that extensively queried loud sound exposure during the previous 12 months. DPOAEs were collected at three f2s (1, 2, and 4 kHz) over a range of L2s. DPOAE stimulus level began at 80 dB forward-pressure level and decreased in 10 dB steps. Two-channel ABRs were collected in response to click stimuli and 4 kHz tone bursts; one channel used an ipsilateral mastoid electrode and the other an ipsilateral tympanic membrane electrode. ABR stimulus level began at 90 dB nHL and was decreased in 10 dB steps. Amplitudes of waves I and V of the ABR were analyzed.ResultsA statistically significant relationship between ABR wave I amplitude and NEB was found for clicked-evoked ABRs recorded at a stimulus level of 90 dB nHL using a mastoid recording electrode. For this condition, ABR wave I amplitudes decreased as a function of NEB. Similar systematic trends were present for ABRs collected in response to clicks and 4 kHz tone bursts at additional suprathreshold stimulation levels (≥70 dB nHL). The relationship weakened and disappeared with decreases in stimulation level (≤60 dB nHL). Similar patterns were present for ABRs collected using a tympanic membrane electrode. However, these relationships were not statistically significant and were weaker and more variable than those collected using a mastoid electrode. In contrast to the findings for ABR wave I, wave V amplitude was not significantly related to NEB. Furthermore, there was no evidence of a systematic relationship between suprathreshold DPOAEs and NEB.ConclusionsA systematic trend of smaller ABR wave I amplitudes was found in normal-hearing human ears with greater amounts of voluntary NEB in response to suprathreshold clicks and 4 kHz tone bursts. These findings are consistent with the data from previous work completed in animals, where the reduction in suprathreshold responses was a result of deafferentation of high-threshold/low-spontaneous rate auditory nerve fibers. These data suggest that a similar mechanism might be operating in human ears after exposure to high sound levels. However, evidence of this damage is only apparent when examining suprathreshold wave I amplitude of the ABR. In contrast, suprathreshold DPOAE level was not significantly related to NEB. This was expected, given noise-induced auditory damage findings in animal ears did not extend to the outer hair cells, the generator for the DPOAE response.