Electroanalytical Tools and Biochemical Assays to Measure the Impact of Noise on Dopamine Neurotransmission in the Central Auditory Pathway

In the United States, loss of hearing impacts approximately 48.1 million people. The cumulative effects of noise are experienced in every area of society whether occupational, environmental, or through aging. Previous work has reported changes in dopamine receptor gene expression following acoustic trauma, suggesting a possible role of dopamine in auditory processing. This conclusion is supported by recent data that showed patients suffering from Parkinson’s disease (a condition associated with dopamine depletion) exhibit deficits in auditory processing. Thus, the present work focuses on the role of dopamine neurotransmission within the central auditory pathway and how it’s impacted by noise exposure. Characterizing the complexities of neurotransmission requires elegant methods of inquiry, regarding both the neurotransmitter and neuron physiology. Fast scan cyclic voltammetry (FSCV) with carbon fiber microelectrodes is uniquely well-suited for real time neurochemical measurement because it has the speed, selectivity, sensitivity, and the spatial resolution needed for such measurements. Immunoassays on the other hand provides information about the neural protein receptors distribution and levels. In this work, dopamine neurotransmission release and uptake events are characterized and quantified with FSCV in the inferior colliculus in vitro and in vivo comparing sound exposed and control groups. Additionally, immunocytochemistry (ICC) and Western blot are utilized to evaluate the effects that damaging sound on dopamine receptors within the inferior colliculus. The combination of FSCV and immunoassays provide a comprehensive examination of the role of dopamine and the repercussions of noise in the central auditory pathway

Evaluating changes in reactive oxygen species (ROS) as a plausible mechanism underlying the effect of noise on dopamine release

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