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.
Training enables adult humans to rapidly adapt their sound localization abilities to unilateral hearing loss by combining different strategies that rely on partially distinct neurophysiological substrates.
Veterans with PTSD show increased attention to a history of unexpected outcomes during loss learning, both as measured by computational model-derived behavioral parameters and in increased neural signaling in amygdala and insula.
Developmental defects of the cochlea caused by dysregulation of sonic hedgehog signaling are the potential etiology for hearing loss in a group of ciliopathies with defective ciliogenesis.
Mild-to-moderate sensorineural hearing loss causes changes in the neurophysiological functioning that emerge during adolescence, as suggested by both cross-sectional and longitudinal designs.
Rat orbitofrontal cortex is required to accurately represent outcome distributions, whereas basolateral amygdala is necessary for the facilitation of learning in response to surprising events.
Developmental hearing loss causes perceptual deficits that are best explained by degraded auditory cortical encoding that is recorded during task performance.
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.
