Faculty Advisor

Aaron K. Apawu

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Excessive exposure to noise has been implicated in hearing loss but the mechanism by which this happens remains unknown. Dopamine, an important neurotransmitter involved in learning and reward-related behaviors has also been reported in the central auditory pathways, suggesting its role in auditory processes. For example, dopamine is found in the inferior colliculus, a principal integration center for auditory responses, and is reported to modulate auditory processes. A recent study has shown that loud noise exposure decreases gene expression for tyrosine hydroxylase (a rate-limiting enzyme in the synthesis of dopamine) in the inferior colliculus, implying diminished dopamine levels. On another hand, excessive production of reactive oxygen species (ROS) is a major contributor to noise-induced hearing loss. ROS can also modulate neuronal processes, including synaptic dopamine release. Thus, we hypothesize that loud noise would trigger overproduction of ROS and in turn attenuate dopamine release in the inferior colliculus. The present work evaluates changes in the ROS, hydrogen peroxide (H2O2) as a plausible mechanism underlying the effect of noise on the dopamine system in the inferior colliculus. Following noise exposure (118 dB sound pressure level at 1/3 octave band for four hours) synaptic changes in H2O2 were assessed with fast-scan cyclic voltammetry (FSCV) in brain slices from adult Sprague Dawley rats and compared to their controls (triangular waveform at a carbon-fiber microelectrode surface between +0.2 V and +1.3 V at a scan rate of 400 V/s). Furthermore, intracellular changes in H2O2 was evaluated using H2O2 assay (National Diagnostics) following noise exposure. Overall, the combination of FSCV and H2O2 assay revealed changes that suggest ROS mediates noise induced alterations in the dopamine system in the inferior colliculus.


This presentation is a finalist for the Graduate Natural and Health Sciences Research Excellence Award