Pou3f4‐expressing otic mesenchyme cells promote spiral ganglion neuron survival in the postnatal mouse cochlea
| Autor: | Meaghan L. Macrae, Ronna Hertzano, Katherine M. Rangoussis, Mansa Gurjar, Kevin Rose, Thomas M. Coate, Paige M. Brooks |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cell Survival Neurogenesis Mesenchyme Population Nerve Tissue Proteins Biology Article Mesoderm Mice 03 medical and health sciences 0302 clinical medicine otorhinolaryngologic diseases medicine Animals Inner ear Axon education Spiral ganglion Mice Knockout Neurons education.field_of_study General Neuroscience Axon extension Cochlea Cell biology Mice Inbred C57BL 030104 developmental biology medicine.anatomical_structure POU Domain Factors Knockout mouse Middle ear sense organs Spiral Ganglion 030217 neurology & neurosurgery |
| Zdroj: | J Comp Neurol |
| ISSN: | 1096-9861 0021-9967 |
| DOI: | 10.1002/cne.24867 |
| Popis: | During inner ear development, primary auditory neurons named spiral ganglion neurons (SGNs) are surrounded by otic mesenchyme cells, which express the transcription factor Pou3f4. Mutations in Pou3f4 are associated with DFNX2, the most common form of X-linked deafness and typically include developmental malformations of the middle ear and inner ear. It is known that interactions between Pou3f4-expressing mesenchyme cells and SGNs are important for proper axon bundling during development. However, Pou3f4 continues to be expressed through later phases of development, and potential interactions between Pou3f4 and SGNs during this period had not been explored. To address this, we documented Pou3f4 protein expression in the early postnatal mouse cochlea and compared SGNs in Pou3f4 knockout mice and littermate controls. In Pou3f4y/- mice, SGN density begins to decline by the end of the first postnatal week, with approximately 25% of SGNs ultimately lost. This period of SGN loss in Pou3f4y/- cochleae coincides with significant elevations in SGN apoptosis. Interestingly, this period also coincides with the presence of a transient population of Pou3f4-expressing cells around and within the spiral ganglion. To determine if Pou3f4 is normally required for SGN peripheral axon extension into the sensory domain, we used a genetic sparse labeling approach to track SGNs and found no differences compared with controls. We also found that Pou3f4 loss did not lead to changes in the proportions of Type I SGN subtypes. Overall, these data suggest that otic mesenchyme cells may play a role in maintaining SGN populations during the early postnatal period. |
| Databáze: | OpenAIRE |
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