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.
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.
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.
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 hearing loss causes perceptual deficits that are best explained by degraded auditory cortical encoding that is recorded during task performance.
In Drosophila, the loss of Frataxin causes iron accumulation in the nervous system, which in turn enhances sphingolipid synthesis and activation of PDK1 and Mef2, which leads to neurodegeneration.
The aged human auditory cortex shows preserved tonotopy, but temporal modulations are represented with a markedly broader tuning, highlighting decreased temporal selectivity as a hallmark of the aging auditory cortex.
