A comprehensive battery of behavioral, electrophysiological and functional MRI techniques has allowed the development of a data-driven conceptual model of the tinnitus-hyperacusis network.

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.

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.

Autism-associated iPSC-derived neurons mutant in CNTN5 or EHMT2 are hyperactive.

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.

Mitogen-activated protein kinase phosphatase 1 (DUSP1) deficiency causes early redox imbalance and increased inflammatory response in the cochlea, leading to cell loss and progressive neurosensory hearing loss.