Artikel
Cochlear function and gross morphology obtained from a genetically induced hypothyroid mouse strain
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Veröffentlicht: | 22. September 2005 |
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Gliederung
Text
Thyroid hormone is essential for the differentiation of cochlear structures. The mouse strain used in our experiment was genetically manipulated and revealed the clinical symptoms of hypothyroidism including enlarged thyroid glands and elevated T3/T4 blood levels. Objective of this study was to examine the effects of the thyroid receptor manipulation on cochlear function and gross morphology.
Mice, 8-10 weeks of age were used in the experiments. Cochlear function was determined by measuring auditory compound action potential thresholds and tone on tone masking curves. In addition to functional testing, gross morphology was determined using the hemicochlea preparation and from 5μm slices cut with a microtome after Araldite Resin embedding. A hemicochlea is a cochlea cut along its mid modiolar plane and allows capturing images of cochlear cross sections. Cochlear dimension were measured using the images captured and NIH-image software. Spiral ganglion cells were counted in wild type and homocygotes. Cochlear function was significantly different in homocygotes when compared to its corresponding wild types. CAP-thresholds were elevated and tone on tone masking experiments showed reduced frequency selectivity.
Gross morphology was similar in homocygotes and wildtype animals as determined in the hemicochlea preparation. However, the spiral ganglion cell counts seemed to be lower in the homocygotes.
Although manipulation of the thyroid receptor did not alter cochlear gross morphology it compromised cochlear function. One may argue that the changes observed in cochlear function result from a smaller number of spiral ganglion cells.