Presentation (Project) Title

Administration of BK Channel Agonist to Reduce Behavioral and Neural Manifestations of Tinnitus in Mice after Induced Acoustic Trauma

Mentor Information

Joseph Walton (Department of Communication Sciences and Disorders)

Presentation Format

Event

Abstract

Tinnitus is a hearing disorder affecting approximately one third of all adults, and unfortunately has no FDA approved curative treatments. The deafferentation of central auditory structures as a result of ARHL or acoustic trauma (AT) causes a reduction in auditory sensory input. This then causes compensatory shifts in the balance of excitation and inhibition of the firing rate of the neurons within the CAS, which most often translates to hyperactivity. One particular BK channel modulator, known as CS0022, has been studied for its effect on hyper-excitability and inhibition in animal models. As a result, this study seeks to investigate this BK channel modulator therapy further and examine its effects on tinnitus in order to support its advancement and clinical usage. Auditory Steady State Responses (ASSRs) are electrophysiologic responses that display hearing sensitivity by evoking periodic amplitude-modulated tones (AM tones). They elicit steady state responses through neural phase-locking, which demonstrates auditory perceptive abilities. The study’s first objective is to examine the effects of AT on ASSR responses, as it is hypothesized that AT suppresses neural phase-locking abilities. The study’s second objective is to examine the effect of CS0022 on the ASSRs of animals with AT-induced tinnitus, as it is hypothesized that CS0022 would enhance neural phase locking abilities. The data demonstrated that animals with tinnitus generally exhibited decreases in ASSR peak amplitudes following AT and increases in ASSR amplitudes following CS0022 administration. These findings suggest that this pharmaceutical treatment may serve as a potential therapeutic in suppressing tinnitus symptoms.

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Administration of BK Channel Agonist to Reduce Behavioral and Neural Manifestations of Tinnitus in Mice after Induced Acoustic Trauma

Tinnitus is a hearing disorder affecting approximately one third of all adults, and unfortunately has no FDA approved curative treatments. The deafferentation of central auditory structures as a result of ARHL or acoustic trauma (AT) causes a reduction in auditory sensory input. This then causes compensatory shifts in the balance of excitation and inhibition of the firing rate of the neurons within the CAS, which most often translates to hyperactivity. One particular BK channel modulator, known as CS0022, has been studied for its effect on hyper-excitability and inhibition in animal models. As a result, this study seeks to investigate this BK channel modulator therapy further and examine its effects on tinnitus in order to support its advancement and clinical usage. Auditory Steady State Responses (ASSRs) are electrophysiologic responses that display hearing sensitivity by evoking periodic amplitude-modulated tones (AM tones). They elicit steady state responses through neural phase-locking, which demonstrates auditory perceptive abilities. The study’s first objective is to examine the effects of AT on ASSR responses, as it is hypothesized that AT suppresses neural phase-locking abilities. The study’s second objective is to examine the effect of CS0022 on the ASSRs of animals with AT-induced tinnitus, as it is hypothesized that CS0022 would enhance neural phase locking abilities. The data demonstrated that animals with tinnitus generally exhibited decreases in ASSR peak amplitudes following AT and increases in ASSR amplitudes following CS0022 administration. These findings suggest that this pharmaceutical treatment may serve as a potential therapeutic in suppressing tinnitus symptoms.