Age and hearing loss effects on subcortical neural encoding

PROJECT SUMMARY Speech recognition difficulties are common for older adults and those with age-related hearing loss (ARHL), particularly in complex environments. Maladaptive hyperexcitability in the central auditory system, a form of central gain, is known to occur with age and hearing loss and may contribute to altered temporal processing and subsequent speech-in-noise (SIN) deficits. Studies of central gain in humans often focus on cortical hyperactivity, yet research suggests that subcortical hyperactivity, notably exaggerated encoding of sound onsets and low-frequency amplitude modulation envelopes (like those common in speech), may be present in the auditory midbrain of older and hearing-impaired adults and exert a larger influence on SIN difficulties than previously thought. However, we currently lack a clear understanding of the contexts in which subcortical hyperactivity exists in age and ARHL and how it relates to behavior. This complicates long-term efforts to develop pharmaceutical and behavioral interventions to ameliorate SIN deficits. The overarching goal of the proposed research is to characterize how hypersensitivities to stimulus onsets and modulation envelopes localized to the auditory midbrain are (1) more prevalent for older than younger adults, (2) related to inferior colliculus structure, (3) predicted by hearing loss in older adults (independently of age), and (4) associated with SIN deficits. Experiments use an innovative combination of electrophysiology, structural neuroimaging, and source localization to characterize neural responses arising from subcortical generator sites (e.g. inferior colliculus) in both quiet and noise. To quantify hyperresponsivities in the midbrain relative to the periphery, inferior colliculus responses are normalized auditory nerve responses. Aim 1 examines whether hyperactivity is more prevalent in older adults relative to younger adults, whether diminished cochlear compression associated with ARHL leads to enhanced envelope encoding in quiet, and assesses how midbrain microstructural characteristics that have been associated with GABAergic changes (e.g. longitudinal relaxation time, R1) relate to hypersensitivity and potentially mediate age effects. Aim 2 examines how midbrain hypersensitivity predicts behavior, testing the hypothesis that greater hypersensitivity benefits perception in quiet (e.g., better amplitude modulation (AM) discrimination in quiet) but not perception in noise (e.g., poorer performance on SIN tests, poorer AM discrimination in noise). Results can advance our understanding of the contexts in which envelope and sound onset hyperresponsivities are present in the subcortical auditory system, how best to quantify it, and whether it alternately benefits or impedes perception. Findings will inform future studies of subcortical neural hyperactivity and not only improve our understanding of SIN difficulties of older adults, but also determine the extent to which clinical interventions need to consider declines in subcortical structure and function. With the aging (and hearing-impaired) population growing yearly, this research has high