Genetic deficits in auditory sensory transduction evoke changes in development and maturation of synapses between inner hair cells and spiral ganglion neurons, which can be partially recovered using inner ear gene therapy.

Damage to the synapses connecting hair cells to the auditory nerve leads to undetected hearing impairments.

Targeted mutations in a Ca²⁺-binding site of otoferlin, a transmembrane protein of synaptic vesicles defective in a recessive form of deafness, reveal its Ca²⁺ sensor role both for vesicle fusion and vesicle pool replenishment.

Ultrastructural and imaging studies of cochlear ribbon synapses demonstrate cis- and trans-synaptic molecular and structural effects in the absence of the AMPA-type glutamate receptor subunit GluA3 during mouse development in ambient sound levels.

Dynamic regulation of feedforward inhibition from parvalbumin-expressing inhibitory neurons is linked to the gradual restoration of cortical sensory processing following auditory nerve damage.

The response from discrete stages of the early auditory pathway can be measured by subtle manipulations to long-form natural speech stimuli paired with deconvolution analysis of electroencephalography data.

Overexpression of the growth factor neurotrophin-3 helps to repair noise-induced damage in the mouse inner ear by promoting the regeneration of damaged synapses.

Ear canal EEG and pupillometry reveal disordered temporal processing in adults with normal hearing who struggle to understand conversations in noisy backgrounds.

Structural basis and molecular mechanism of how molecular chaperone Hsp27 specifically captures phosphorylated Tau and prevents it from abnormal aggregation.

The BMAL1-REV-ERB axis controls expression of complement C4b expression and microglial synaptic phagoctyosis, providing a link between cellular circadian clock function and synaptic regulation.