Hearing Loss: New Study Reveals Brain Pathways to Healing

Researchers have studied how the brain controls hearing through nerves called efferents, which send signals to the cochlea. They found that in the long term, these signals help compensate for hearing loss by making sounds more audible. However, this adaptation can cause side effects such as tinnitus and oversensitivity to sound. In the short term, however, these nerves do not adjust hearing based on the brain’s level of attention. These findings could help in the development of new treatments for hearing problems.

The cochlea, the part of the inner ear responsible for hearing, uses sensory hair cells to detect sound waves in the air and then convert them into electrical signals that the brain can process. Most cochlear nerves carry information from the cochlea to the brain, but about 5 percent send signals in the opposite direction: from the brain to the cochlea.

The exact role of these fibers has been a mystery, because researchers have struggled to measure cochlear activity in humans or animals while they are awake.

In the short term, they are thought to help adjust hearing to a person's attention span, while in the long term, they may protect against damage from loud sounds. However, testing these functions has been difficult because directly measuring the effects of efferent signals in awake animals is a technical challenge.

To better understand the role of these efferent fibers, the researchers studied mice, both awake and anesthetized. The study was made possible by a novel imaging tool that allowed the researchers to capture real-time images of the cochlea in awake animals for the first time.

They focused on a specific group of nerves called the medial olivocochlear (MOC) efferent system, which communicates with specialized cells in the cochlea. The goal was to analyze how these nerves affect sound amplification within the inner ear.

The scientists used two main approaches: long-term (chronic) effects and short-term (immediate) effects. To understand how the loss of nerve signals alters hearing over time, the researchers used mice genetically modified to disable certain types of nerve connections.

In one group, they removed only the afferent signals (which carry information from the cochlea to the brain), using mice called VGLUT3-/-. In another group, they removed both the afferent and efferent signals, using mice called VGLUT3-/- Alpha9-/-.

When they compared these groups, they found that sound amplification in the cochlea increased when only the afferents were removed, but only if the efferents were functioning normally. This suggests that the medial olivocochlear efferent system may act to compensate for the loss of auditory signals over time.

To investigate whether the medial olivocochlear efferent system adjusts hearing in real time, according to the state of the brain (for example, whether the animal is more or less alert), the scientists measured vibrations in the cochlea while monitoring changes in the size of the mice’s pupils.

Pupil size is an indicator of the brain’s level of alertness. However, the results showed that cochlear amplification did not vary with changes in brain state. On the other hand, effects of these changes were observed in a part of the brain called the inferior colliculus, which processes sounds after they pass through the cochlea and brainstem.

The results indicate that the medial olivocochlear efferent system plays an important role in regulating hearing over the long term, but does not respond quickly to changes in the brain’s level of attention.

This means that it may help compensate for hearing loss over time, making sounds more audible when there are fewer signals reaching the brain. However, this compensation may also have side effects, such as increasing the likelihood of symptoms such as tinnitus (perceiving sounds that are not there) and hyperacusis (excessive sensitivity to sounds).

This finding helps to better understand the mechanisms involved in hearing and may pave the way for new approaches to treating hearing loss and its associated symptoms.

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The medial olivocochlear efferent pathway potentiates cochlear amplification in response to hearing loss

Patricia M. Quiñones, Michelle Pei, Hemant Srivastava, Ariadna Cobo-Cuan, Marcela A. Morán, Bong Jik Kim, Clayton B. Walker, Michael J. Serafino, Frank Macias-Escriva, Juemei Wang, James B. Dewey, Brian E. Applegate, Matthew J. McGinley and John S. Oghalai

Journal of Neuroscience. 21 February 2025, e2103242025;

DOI: 10.1523/JNEUROSCI.2103-24.2025

Abstract: 

The mammalian cochlea receives efferent feedback from the brain. Many functions for this feedback have been hypothesized, including on short timescales, such as mediating attentional states, and long timescales, such as buffering acoustic trauma. Testing these hypotheses has been impeded by an inability to make direct measurements of efferent effects in awake animals. Here, we assessed the role of the medial olivocochlear (MOC) efferent nerve fibers on cochlear amplification by measuring organ of Corti vibratory responses to sound in both sexes of awake and anesthetized mice. We studied long-term effects by genetically ablating the efferents and/or afferents. Cochlear amplification increased with deafferentation using VGLUT3-/- mice, but only when the efferents were intact, associated with increased activity within OHCs and supporting cells. Removing both the afferents and the efferents using VGLUT3-/- Alpha9-/- mice did not cause this effect. To test for short-term effects, we recorded sound-evoked vibrations while using pupillometry to measure neuromodulatory brain state. We found no state dependence of cochlear amplification or of the auditory brainstem response. However, state dependence was apparent in the downstream inferior colliculus. Thus, MOC efferents upregulate cochlear amplification chronically with hearing loss, but not acutely with brain state fluctuations. This pathway may partially compensate for hearing loss while mediating associated symptoms, such as tinnitus and hyperacusis.