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

Mechanically induced injury of zebrafish lateral-line organs shares key features of damage observed in noise-exposed mammalian ears, such as inflammation and synapse loss, yet, unlike mammals, rapidly repairs following damage.

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.

Based on the animal’s recent history of sound exposure, cholinergic auditory brainstem neurons dynamically regulate dopamine synthesis for inhibitory feedback to the inner ear.

Central damage and sensory deprivation caused by noise-induced hearing loss in the pre-symptomatic Alzheimer's disease (AD) phase can compromise auditory cortex-hippocampal circuitry, targeting common pathogenetic pathways, thereby accelerating onset and progression of AD phenotype.

SLC7A8 a neutral amino acid transporter has a key role in the maintenance of hearing during aging and its absence causes early onset of hearing loss.

Chronic two-photon calcium imaging, optogenetics, and operant behavioral approaches were leveraged to show that hyperactivity, hyperresponsivity, and hypersynchronization in auditory cortex neural ensembles can account for auditory hypersensitivity following acoustic trauma.

A method of generating comprehensive maps of cochlear cells was created and enabled researchers to study characteristics of cellular damage in aged and noise-exposed inner ear.

Mice that successfully avoid developing tinnitus despite exposure to excessive noise show spontaneous recovery of KCNQ2/3 potassium channel activity associated with a reduction in HCN channel activity in auditory brainstem neurons.

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