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Gene expression profiles along the tonotopic axis of the mouse cochlea during neonatal development

ABSTRACT: The cochlear duct is tonotopically organized, such that the basal cochlea responds more sensitively to high frequency sounds and the apical cochlea to low frequency sounds. In effort to understand how the tonotopic organization is established in mammals, we searched for genes that are differentially expressed along the tonotopic axis during neonatal development.

ORGANISM(S): Mus musculus

PROVIDER: GSE34187 | GEO | 2011/12/13

SECONDARY ACCESSION(S): PRJNA149701

REPOSITORIES: GEO

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Gene expression profiles along the tonotopic axis of the mouse cochlea during neonatal development

Project description:The cochlear duct is tonotopically organized, such that the basal cochlea responds more sensitively to high frequency sounds and the apical cochlea to low frequency sounds. In effort to understand how the tonotopic organization is established in mammals, we searched for genes that are differentially expressed along the tonotopic axis during neonatal development. Eighty temporal bones were dissected from C57BL/6 mice at P0 and P8. The cochlear tissues were divided into three equal pieces representing the basal, middle and apical turns, and pooled separately. Six total RNA from the pooled samples were applied to 6 GeneChips.

2011-12-13 | E-GEOD-34187 | biostudies-arrayexpress

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Project description:A cardinal feature of the auditory pathway is frequency selectivity represented in the form of a tonotopic map from the cochlea to the cortex. The molecular determinants of the auditory frequency map are unknown. Here, we discovered that the transcription factor ISL1 regulates features of auditory neurons, including the formation of the spiral ganglion neuron (SGN) and peripheral and central processes that shape the tonotopic representation of the auditory map. We selectively knocked out Isl1 in auditory neurons using Neurod1Cre strategies. In the absence of Isl1, SGNs migrate into the central cochlea and beyond. The cochlear wiring is profoundly reduced and disrupted. The central axons of Isl1 mutants lose their topographic projections and segregation at the cochlear nucleus. Transcriptome analysis of SGNs shows that Isl1 regulates neurogenesis, axonogenesis, migration, and the functional properties of neurons. Surprisingly, notable auditory processing features are preserved despite the significant hearing impairment, revealing central auditory pathway resilience and plasticity in mutant mice. Mutant mice demonstrate altered acoustic startle reflex, prepulse inhibition, characteristics of compensatory neural hyperactivity centrally. Our findings show that the Isl1 is one of the obligatory factors required to sculpt auditory structural and functional tonotopic maps. Still, upon Isl1 deletion, the ensuing compensatory plasticity of the auditory pathway does not suffice to overcome developmental changes at the peripheral sensory organ.

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