Brain Struct Funct

Abstract

Loud noise frequently results in hyperacusis or hearing loss (i.e., increased or decreased sensitivity to sound). These conditions are often accompanied by tinnitus (ringing in the ears) and changes in spontaneous neuronal activity (SNA). The ability to differentiate the contributions of hyperacusis and hearing loss to neural correlates of tinnitus has yet to be achieved. Towards this purpose, we used a combination of behavior, electrophysiology, and imaging tools to investigate two models of noise-induced tinnitus (either with temporary hearing loss or with permanent hearing loss). Manganese (Mn|) uptake was used as a measure of calcium channel function and as an index of SNA. Manganese uptake was examined in vivo with manganese-enhanced magnetic resonance imaging (MEMRI) in key auditory brain regions implicated in tinnitus. Following acoustic trauma, MEMRI, the SNA index, showed evidence of spatially dependent rearrangement of Mn| uptake within specific brain nuclei (i.e., reorganization). Reorganization of Mn| uptake in the superior olivary complex and cochlear nucleus was dependent upon tinnitus status. However, reorganization of Mn| uptake in the inferior colliculus\ua0was dependent upon hearing sensitivity. Furthermore, following permanent hearing loss, reduced Mn| uptake was observed. Overall, by combining testing for hearing sensitivity, tinnitus, and SNA, our data move forward the possibility of discriminating the contributions of hyperacusis and hearing loss to tinnitus.R21 EY021619/EY/NEI NIH HHS/United StatesT42 OH008455/OH/NIOSH CDC HHS/United StatesT42 OH008455/National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention/I01 RX001095/RX/RRD VA/United Statesunrestricted grant/Research to Prevent Blindness/1I01RX001095-01U.S/U.S. Department of Veterans Affairs/EY021619/National Institutes of Health/2019-06-01T00:00:00Z29488007PMC6129978631