P071 The Role of Descending Inferior Colliculus Projections to the Cochlear Nucleus in the Hyperactivity Underlying Tinnitus
Katherine Doxey*1, Timothy Balmer2, Sharon Crook1
1School of Mathematical and Statistical Sciences, Arizona State University, Tempe, United States 2School of Life Sciences, Arizona State University, Tempe, United States
*Email: kedoxey@asu.edu
Introduction
Tinnitus is the perception of a sound without the presence of auditory stimuli. Over 2.5 million veterans are currently receiving disability benefits for a tinnitus diagnosis [1] and the likelihood of veterans screening positive for posttraumatic stress disorder (PTSD) increases with severity of tinnitus [2]. We focus on tinnitus from high-frequency hearing loss that is associated with exposure to loud noise and is perpetuated by neuronal hyperactivity in the dorsal cochlear nucleus (DCN). In this study, we test the hypothesis that descending projections from the inferior colliculus (IC) cause hyperexcitability of frequencies that are no longer encoded by the bottom-up sensory signals after damage to the cochlea [3].
Methods We implement a network model of central auditory processing that consists of 200 fusiform cells that receive tonotopic excitatory input from 200 spiral ganglion neurons (SGN) and lateral inhibitory input from 200 interneurons. We implement the descending IC projections with 200 cells that provide excitatory input to the fusiform cells. Auditory input is modeled as a depolarization of SGN neurons and hearing loss is modeled as reduced depolarization of SGN neurons at the highest frequency range. Each cell is an Izhikevich model neuron with regular spiking dynamics [4]. We characterize the dynamics of the network by applying a pure tone stimulus and simulating either normal hearing or hearing loss. Results Without descending IC projections, we confirm that loss of auditory nerve input at the high frequency range produces aberrant excitation at adjacent frequencies of the tonotopic map, i.e. tinnitus. With descending IC projections, we demonstrate that the signal to noise ratio increases as well as the hyperexcitability of the adjacent frequencies. Discussion A significant barrier to the treatment of tinnitus is the lack of knowledge on the source of the hyperexcitability; understanding the interactions between the DCN and IC in the central auditory pathway is essential to the development of physiology-based treatment to target the appropriate circuit elements. Our model shows that the descending IC projections result in hyperexcitability of high frequencies that are not encoded after hearing loss. To better understand these mechanisms, future work will involve extending the DCN model network to include narrowband and wideband inhibitors that contribute to processing pure tone, broadband, and notch noise stimuli.
Acknowledgements This research is supported by DARPA YFA. References 1.Annual Benefits Report 2021- Veterans Benefits Administration Reports. https://www.benefits.va.gov/REPORTS/abr/ 2.Prewitt, A., Harker, G., Gilbert, T. A., et al. (2021). Mental Health Symptoms Among Veteran VA Users by Tinnitus Severity:A Population-based Survey. Military Medicine, 186(Suppl 1), 167–175. 3.Gerken, G. M. (1996). Central tinnitus and lateral inhibition: An auditory brainstem model. Hearing Research, 97(1), 75–83. 4.Izhikevich, E. M. (2003). Simple model of spiking neurons. IEEE Transactions on Neural Networks, 14(6), 1569–1572.
