Kenneth E. Hancock

The paper identifies neural and autonomic predictors of future listening errors in a sustained auditory task.

The paper investigates whether neural and behavioral markers of distraction suppression correlate with tinnitus severity, finding no such association.

This paper measures neural synchronization to different sound timescales in human listeners to determine how distraction affects auditory processing.

This study shows that modulating parvalbumin-expressing neurons in the auditory cortex can adjust loudness perception and reverse auditory hypersensitivity in mice.

The paper identifies objective signatures of tinnitus and auditory hypersensitivity disorders through pupil dilation and facial movement analysis in response to sound valence.

The paper identifies facial motion energy (FME) as a sensitive measure of hearing abilities in mice, showing its reliability and ability to decode speech in noise.

This study investigates how changes in parvalbumin-expressing inhibitory interneurons in the auditory cortex affect loudness perception and hyperacusis in mice.

This study shows that acoustic trauma leads to non-homeostatic gain changes in auditory cortex neurons, contributing to hypersensitivity to sound.

This study shows mechanical overstimulation causes acute injury and synapse loss in zebrafish neuromasts, but recovery occurs rapidly.

The paper identifies that motor preparatory inputs activate auditory corticothalamic neurons before orofacial movements in mice.

The paper identifies neural signatures of poor multi-talker speech perception in adults with normal hearing, linking it to phase locking to frequency modulation cues and cognitive listening effort.

The paper uses imaging techniques to map sound frequency organization in mouse auditory cortex fields, identifying new areas and clarifying tonotopic organization.

The paper optimizes optogenetic stimulation protocols in auditory corticofugal neurons using closed-loop spike feedback to enhance or suppress midbrain firing rates.

The paper shows that auditory cortex projection neurons adjust their gain after cochlear nerve damage, leading to increased excitability and potential network dysfunction in tinnitus.