Hui Hong, Ph.D.
Meet the Researcher
Hong received her doctorate in communication sciences and disorders from Northwestern University. Following postdoctoral training at Oregon Health & Science University, she became an assistant professor at the Bellucci Translational Hearing Center at Creighton University. Hong is a 2026 recipient of an Elizabeth M. Keithley, Ph.D. Early Stage Investigator Award.
When we think about hearing, we often picture sound traveling from the ear to the brain – a one-direction sensory pathway. However, hearing also involves a lesser-known feedback system called the auditory efferent system, which sends signals from the brain back to the ear. This system helps regulate how we hear in different sound environments and plays a protective role for the inner ear. Hearing loss is a prevalent health issue in modern society and is closely associated with other auditory disorders.
Most research on hearing loss has focused on the sensory pathway. In contrast, much less is known about how the efferent system contributes to these conditions. This project focuses on the lateral olivocochlear (LOC) neurons, the most abundant auditory efferent neurons, to understand how their function changes after noise-induced hearing loss. These changes include both the neurons’ own activity and the inputs that regulate that activity. A key question is whether the observed changes are driven directly by noise exposure or by the resulting hearing loss.
To address this, we will compare LOC function following noise-induced hearing loss with that following non-noise-induced hearing loss, the latter produced by targeted ear lesions. Our approach combines whole-cell patch-clamp electrophysiology, a classic technique for recording the activity of individual neurons, with state-of-the-art optogenetics, which allows precise control and study of neuronal inputs.
This research will deepen our understanding of how hearing loss impacts the auditory efferent system and help resolve inconsistencies observed in clinical studies on efferent involvement in conditions such as central auditory processing disorder, hyperacusis, and tinnitus. Ultimately, these insights will guide clinicians in refining therapeutic interventions by pinpointing dysfunctions within the brain and suggesting strategies for functional recovery. They will also help tailor treatments based on the underlying cause of hearing loss.
My long-term goal is to understand the function of the auditory efferent system in health and disease and to develop targeted interventions for improved hearing therapies. Moreover, this study examines how various forms of hearing loss affect the LOC efferent system, providing insights that can guide clinicians in developing tailored treatment plans based on the underlying cause of the hearing loss. For instance, noise-induced hearing loss may elicit a stronger neuroinflammatory response in LOC neurons compared to hearing loss caused by inner ear lesions. As a result, clinical trials could explore whether combining anti-inflammatory drugs and ion channel modulators with hearing devices provides an effective approach to addressing noise-induced hearing loss.
The auditory efferent system— particularly the LOC system— has remained an enigma for decades. Recent studies have advanced knowledge of LOC neurons under normal conditions and in the context of both noise-induced and congenital hearing loss. Emerging evidence suggests that LOC neurons contribute to the restoration of auditory nerve activity after noise damage. However, the electrophysiological basis underlying this restorative function remains unknown. Our lab specializes in auditory electrophysiology and has previously identified unique firing patterns of healthy LOC neurons along with their upstream synaptic inputs. Building on this foundation, it is critical to determine how this LOC function changes following hearing loss and whether these changes exert adaptive effects within the cochlea.
During my postdoctoral training I observed bursting calcium signals in LOC neurons under two-photon microscopy. For a long time, we had detected burst firing with recording pipettes, but there was always uncertainty about whether this activity was a pipette-induced artifact. Seeing the same bursting activity confirmed through non-invasive two-photon imaging was a powerful validation, and it remains one of the most memorable highlights of my research career.
I studied botany and zoology in high school, inspired by an exceptional biology teacher. This early experience sparked my interest in the life sciences and led me to pursue biomedical engineering in college. In my senior year, I had the privilege of joining the lab of an outstanding auditory researcher, where I conducted my honors thesis on the auditory cortex. Since then, I have committed myself to advancing hearing research and have remained dedicated to the auditory field throughout my doctoral studies and beyond.
Both of my grandparents, as well as our family dog, suffered from profound age-related hearing loss. I witnessed firsthand how the loss of hearing disrupted daily life—not only by limiting communication, but also by leading to social withdrawal and emotional isolation. Although both of my grandparents wore hearing aids, they often expressed frustration that these devices did not truly restore their hearing. Over time, they abandoned using them altogether, which only deepened their struggles and further diminished their quality of life. These experiences revealed the urgent need for more effective treatments—interventions that go beyond simply amplifying sound and instead address the complex neural changes underlying hearing loss.
I have over 15 years of experience playing the violin, though I have not yet explored whether this has enhanced my sensitivity to subtle frequency changes, as is often observed in other musicians. I’m also a big red panda fan and dream of studying their auditory system someday.
The Research
Hui Hong, Ph.D. | Creighton University
Peripheral auditory input regulates lateral cochlear efferent system
When we think about hearing, we often picture sound traveling from the ear to the brain—a one-direction sensory pathway. However, hearing also involves a lesser-known feedback system called the auditory efferent system, which sends signals from the brain back to the ear. This system helps regulate how we hear in different sound environments and plays a protective role for the inner ear. Hearing loss is a prevalent health issue in modern society and is closely associated with other auditory disorders. Most research on hearing loss has focused on the sensory pathway. In contrast, much less is known about how the efferent system contributes to these conditions.
This project focuses on the lateral olivocochlear (LOC) neurons, the most abundant auditory efferent neurons, to understand how their function changes after noise-induced hearing loss. These changes include both the neurons’ own activity and the inputs that regulate that activity. A key question is whether the observed changes are driven directly by noise exposure or by the resulting hearing loss. To address this, we will compare LOC function following noise-induced hearing loss with that following non-noise-induced hearing loss, the latter produced by targeted ear lesions.
Our approach combines whole-cell patch-clamp electrophysiology, a classic technique for recording the activity of individual neurons, with state-of-the-art optogenetics, which allows precise control and study of neuronal inputs. This research will deepen our understanding of how hearing loss impacts the auditory efferent system and help resolve inconsistencies observed in clinical studies on efferent involvement in conditions such as central auditory processing disorder, hyperacusis, and tinnitus. Ultimately, these insights will guide clinicians in refining therapeutic interventions by pinpointing dysfunctions within the brain and suggesting strategies for functional recovery. They will also help tailor treatments based on the underlying cause of hearing loss.
Long-term goal: My long-term goal is to understand the function of the auditory efferent system in health and disease and to develop targeted interventions for improved hearing therapies. In addition to investigating cellular and synaptic alterations in LOC neurons associated with noise-induced hearing loss, I will explore potential molecular changes. LOC neurons are neurochemically heterogeneous and may comprise distinct subtypes with varying susceptibility to noise—a critical area of study that could inform gene therapy strategies.
While my current research focuses on central changes in the LOC efferent system, fully understanding its role in health and disease, as well as creating effective interventions, will require experiments at the cochlear level. In vitro and in vivo studies will explore how LOC neurons release diverse neurotransmitters and neuromodulators in the cochlea that exert an effect on the activity of spiral ganglion neurons (SGNs), and how altered LOC activity with hearing loss impacts these release patterns and SGN function. It is also possible that under pathological conditions LOC fibers have rewired to directly affect inner hair cells. This knowledge will offer insights into whether altered efferent modulation is adaptive or pathological, providing a foundation for clinical applications to determine whether enhancing or suppressing LOC activity is more effective in restoring hearing sensitivity after auditory trauma.
My future research will extend beyond noise-induced hearing loss to include congenital hearing loss, ototoxicity-induced hearing loss and age-related hearing loss, all prevalent disorders, examining their impacts on the function of LOC efferent system. These insights will guide the development of tailored hearing therapies for various causes of hearing loss, helping to mitigate the risks of central auditory processing disorder (CAPD), hyperacusis, and tinnitus.
This proposed work has the potential to enhance therapeutic interventions for hearing loss by identifying dysfunctional cell types in the central nervous system and proposing strategies for functional recovery. Targeting the auditory efferent system might be crucial for preventing the onset of CAPD, hyperacusis, and tinnitus following hearing loss. Additionally, patients with hearing restoration devices such as cochlear implants and hearing aids often struggle to hear in noisy environments, partially due to altered efferent activity associated with hearing loss. Current hearing restoration approaches do not address this pathway. LOC neurons exhibit spontaneous burst firing driven by Ca2+ channels, which are highly susceptible to noise-induced hearing loss.
This study aims to identify changes in Ca2+ channels, as well as other voltage- gated, leak, or ligand-gated ion channels, and their collective impact on altered electrical activity in LOC neurons. These channelopathies could serve as therapeutic targets. For instance, modulators of Ca2+ channels could be developed to finely tune LOC neuron activity, offering sufficient protection for the auditory nerve while preventing overcompensation that may lead to pathological effects.
The next step involves developing safe, effective drugs targeting these channelopathies, optimized for oral administration or direct injection into the bloodstream. Clinical trials would then evaluate whether combining these drugs with traditional hearing restoration devices improves patients’ overall hearing experiences and reduces the risk of CAPD, hyperacusis, or tinnitus.
This integrated approach holds promise for more comprehensive hearing therapies. Moreover, this study examines how various forms of hearing loss affect the LOC efferent system, providing insights that can guide clinicians in developing tailored treatment plans based on the underlying cause of the hearing loss. For instance, noise-induced hearing loss may elicit a stronger neuroinflammatory response in LOC neurons compared to hearing loss caused by inner ear lesions. As a result, clinical trials could explore whether combining anti-inflammatory drugs and ion channel modulators with hearing devices provides an effective approach to addressing noise-induced hearing loss.
Recipient of an Elizabeth M. Keithley, Ph.D. Early Stage Investigator Award