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A novel mechanism for F-actin repair is involved in the maintenance of sensory hair cells and hearing function.

Large-scale gene expression analysis of the songbird brain identifies the molecular and cellular features of vocal motor circuits that are altered by the loss of hearing.

The planar polarized organization of vestibular hair cells in the mouse inner ear is determined by the coordinated activities of the STK32A kinase and the transcription factor EMX2 to regulate the orphan receptor GPR156.

Deep neural network modeling of auditory processing identifies distorted cross-frequency interactions as the key problem for the processing of speech in noise after hearing loss.

The imprecise and broad connectivity of retinal inputs during development have the potential to generate large correlations in target neurons that reduce retinotopic information unless suppressed by the special synaptic and circuit properties present at these ages.

Single-nucleus sequencing, anatomy, and physiology reveal heterogeneity among olivocochlear neurons (a group of cells that provide feedback to the inner ear), identify a neuropeptide-enriched subtype, and show that neuropeptide expression changes during postnatal development and after sound exposure.

Single-cell transcriptomic analysis defines hair cell and supporting cell types in the zebrafish inner ear, and reveals homologies with cells in the mammalian ear.

Cells of the mammalian cochlea can be reprogrammed to produce mechanosensory hair cells, but epigenetic changes in the cochlea make this process less efficient with age.

A combination of genetic, electrophysiological, and modeling approaches reveals that presynaptic Rac1 is a key molecule that controls synaptic strength and plasticity by regulating the synaptic vesicle cycle steps controlling the number of fusion competent synaptic vesicles.

In the cochlea, repressor element 1-silencing transcription factor (REST) regulates the expression levels of K_v7.4 and alterations of REST functions result in progressive hearing loss.