Hair Cells

NIH Researchers Show Protein in Inner Ear Is Key to How Cells That Help With Hearing and Balance Are Positioned

By the National Institute on Deafness and Other Communication Disorders (NIDCD)

Line of polarity reversal (LPR) and location of Emx2 within two inner ear structures. Arrows indicate hair bundle orientation. Source: eLife

Line of polarity reversal (LPR) and location of Emx2 within two inner ear structures. Arrows indicate hair bundle orientation. Source: eLife

Using animal models, scientists have demonstrated that a protein called Emx2 is critical to how specialized cells that are important for maintaining hearing and balance are positioned in the inner ear. Emx2 is a transcription factor, a type of protein that plays a role in how genes are regulated. Conducted by scientists at the National Institute on Deafness and Other Communication Disorders (NIDCD), part of the National Institutes of Health (NIH), the research offers new insight into how specialized sensory hair cells develop and function, providing opportunities for scientists to explore novel ways to treat hearing loss, balance disorders, and deafness. The results are published March 7, 2017, in eLife.

Our ability to hear and maintain balance relies on thousands of sensory hair cells in various parts of the inner ear. On top of these hair cells are clusters of tiny hair-like extensions called hair bundles. When triggered by sound, head movements, or other input, the hair bundles bend, opening channels that turn on the hair cells and create electrical signals to send information to the brain. These signals carry, for example, sound vibrations so the brain can tell us what we’ve heard or information about how our head is positioned or how it is moving, which the brain uses to help us maintain balance.

NIDCD researchers Doris Wu, Ph.D., chief of the Section on Sensory Cell Regeneration and Development and member of HHF’s Scientific Advisory Board, which provides oversight and guidance to our Hearing Restoration Project (HRP) consortium; Katie Kindt, Ph.D., acting chief of the Section on Sensory Cell Development and Function; and Tao Jiang, a doctoral student at the University of Maryland College Park, sought to describe how the hair cells and hair bundles in the inner ear are formed by exploring the role of Emx2, a protein known to be essential for the development of inner ear structures. They turned first to mice, which have been critical to helping scientists understand how intricate parts of the inner ear function in people.

Each hair bundle in the inner ear bends in only one direction to turn on the hair cell; when the bundle bends in the opposite direction, it is deactivated, or turned off, and the channels that sense vibrations close. Hair bundles in various sensory organs of the inner ear are oriented in a precise pattern. Scientists are just beginning to understand how the hair cells determine in which direction to point their hair bundles so that they perform their jobs.

In the parts of the inner ear where hair cells and their hair bundles convert sound vibrations into signals to the brain, the hair bundles are oriented in the same direction. The same is true for hair bundles involved in some aspects of balance, known as angular acceleration. But for hair cells involved in linear acceleration—or how the head senses the direction of forward and backward movement—the hair bundles divide into two regions that are oriented in opposite directions, which scientists call reversed polarity. The hair bundles face either toward or away from each other, depending on whether they are in the utricle or the saccule, two of the inner ear structures involved in balance. In mammals, the dividing line at which the hair bundles are oriented in opposite directions is called the line of polarity reversal (LPR).

Using gene expression analysis and loss- and gain-of-function analyses in mice that either lacked Emx2 or possessed extra amounts of the protein, the scientists found that Emx2 is expressed on only one side of the LPR. In addition, they discovered that Emx2 reversed hair bundle polarity by 180 degrees, thereby orienting hair bundles in the Emx2 region in opposite directions from hair bundles on the other side of the LPR. When the Emx2 was missing, the hair bundles in the same location were positioned to face the same direction.

Looking to other animals to see if Emx2 played the same role, they found that Emx2 reversed hair bundle orientation in the zebrafish neuromast, the organ where hair cells with reversed polarity that are sensitive to water movement reside.

These results suggest that Emx2 plays a key role in establishing the structural basis of hair bundle polarity and establishing the LPR. If Emx2 is found to function similarly in humans, as expected, the findings could help advance therapies for hearing loss and balance disorders. They could also advance research into understanding the mechanisms underlying sensory hair cell development within organs other than the inner ear.

This work was supported within the intramural laboratories of the NIDCD (ZIA DC000021 and ZIA DC000085).

Doris Wu Ph.D. is member of HHF’s Scientific Advisory Board, which provides oversight and guidance to our Hearing Restoration Project (HRP) consortium This article was repurpsed with permission from the National Institute on Deafness and Other Communication Disorders. 

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Success of Sensory Cell Regeneration Raises Hope for Hearing Restoration

By St. Jude Children's Research Hospital

Jian Zuo, Ph.D., and his colleagues induced supporting cells located in the inner ear of adult mice to take on the appearance of immature hair cells and to begin producing some of the signature proteins of hair cells.

Jian Zuo, Ph.D., and his colleagues induced supporting cells located in the inner ear of adult
mice to take on the appearance of immature hair cells and to begin producing some of the signature proteins of hair cells.

In an apparent first, St. Jude Children's Research Hospital investigators have used genetic manipulation to regenerate auditory hair cells in adult mice. The research marks a possible advance in treatment of hearing loss in humans. The study appears today in the journal Cell Reports.

Loss of auditory hair cells due to prolonged exposure to loud noise, accidents, illness, aging or medication is a leading cause of hearing loss and long-term disability in adults worldwide. Some childhood cancer survivors are also at risk because of hair cells damage due to certain chemotherapy agents. Treatment has focused on electronic devices like hearing aids or cochlear implants because once lost, human auditory hair cells do not grow back.

"In this study, we looked to Mother Nature for answers and we were rewarded," said corresponding author Jian Zuo, Ph.D., a member of the St. Jude Department of Developmental Neurobiology. "Unlike in humans, auditory hair cells do regenerate in fish and chicken. The process involves down-regulating expression of the protein p27 and up-regulating the expression of the protein Atoh1. So we tried the same approach in specially bred mice."

By manipulating the same genes, Zuo and his colleagues induced supporting cells located in the inner ear of adult mice to take on the appearance of immature hair cells and to begin producing some of the signature proteins of hair cells.

The scientists also identified a genetic pathway for hair cell regeneration and detailed how proteins in that pathway cooperate to foster the process. The pathway includes the proteins GATA3 and POU4F3 along with p27 and ATOH1. In fact, investigators found that POU4F3 alone was sufficient to regenerate hair cells, but that more hair cells were regenerated when both ATOH1 and POU4F3 were involved.

"Work in other organs has shown that reprogramming cells is rarely accomplished by manipulating a single factor," Zuo said. "This study suggests that supporting cells in the cochlea are no exception and may benefit from therapies that target the proteins identified in this study."

The findings have implications for a phase 1 clinical trial now underway that uses gene therapy to restart expression of ATOH1 to regenerate hair cells for treatment of hearing loss.

ATOH1 is a transcription factor necessary for hair cell development. In humans and other mammals, the gene is switched off when the process is complete. In humans, ATOH1 production ceases before birth.

"This study suggests that targeting p27, GATA3 and POU4F3 may enhance the outcome of gene therapy and other approaches that aim to restart ATOH1 expression," Zuo said.

The research also revealed a novel role for p27. The protein is best known as serving as a check on cell proliferation. However, in this study p27 suppressed GATA3 production. Since GATA3 and ATOH1 work together to increase expression of POU4F3, reducing GATA3 levels also reduced expression of POU4F3. When the p27 gene was deleted in mice, GATA3 levels increased along with expression of POU4F3. Hair cell regeneration increased as well.

"Work continues to identify the other factors, including small molecules, necessary to not only promote the maturation and survival of the newly generated hair cells, but also increase their number," Zuo said.

Bradley J. Walters, Ph.D. was a 2012 Hearing Health Foundation Emerging Research Grants recipient. This article was repurpsed with permission. 

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A Balancing Act Before the Onset of Hearing

By Sonja J. Pyott, Ph.D.

Our ability to hear relies on the proper connections between the sensory hair cells in the inner ear and the brain. Activity of the sensory hair cells (red) and these connections ( green) before hearing begins is essential for the proper development of hearing. The research conducted by Sonja J. Pyott, Ph.D., and colleagues investigated the mechanisms that regulate this activity.

Our ability to hear relies on the proper connections between the sensory hair cells in the inner ear and the brain. Activity of the sensory hair cells (red) and these connections ( green) before hearing begins is essential for the proper development of hearing. The research conducted by Sonja J. Pyott, Ph.D., and colleagues investigated the mechanisms that regulate this activity.

The development of the auditory system begins in the womb and culminates in a newborn’s ability to hear upon entering the world. While the age at which hearing begins varies across mammals, the sensory structures of the inner ears are active before the onset of hearing. This activity instructs the maturation of the neural connections between the inner ear and brain, an essential component of the proper development of hearing. However, we still know very little about the mechanisms regulating the activity of these sensory structures and their neural connections, specifically during the critical period just before the onset of hearing.

In our paper, “mGluR1 enhances efferent inhibition of inner hair cells in the developing rat cochlea,” soon to be published in an upcoming issue of The Journal of Physiology, we investigate the role of glutamate, a neurotransmitter, in regulating activity of the sensory structures and their connections in the inner ear before the start of hearing.

Neurotransmitters assist in the communication between neurons and are typically classified as either excitatory or inhibitory based on their action. Excitatory action results in stimulation; inhibitory action assists in the calming of the brain. Our research found that although glutamate typically excites activity, it also elicits inhibitory activity. This dual role for glutamate occurs because it activates two distinct classes of glutamate receptors: ionotropic glutamate receptors (iGluRs) and metabotropic glutamate receptors (mGluRs).

Importantly, this dual activation balances excitatory and inhibitory activity of the sensory structures, a balance of which is likely important in the final refinement of the neural connections between the inner ear and brain prior to the onset of hearing.

As part of future research, we will further investigate the role of mGluRs, one the distinct classes of glutamate receptors, in the development of hearing. We will also investigate if mGluRs balance excitatory and inhibitory activity in the adult inner ear, similar to its role prior to the onset of hearing. Insights into these mechanisms may identify new ways to modulate activity and prevent congenital or acquired hearing loss.

Study coauthor Sonja J. Pyott, Ph.D., was a 2007 and 2008 Hearing Health Foundation Emerging Research Grants recipient.

We need your help supporting innovative hearing and balance science through our Emerging Research Grants program. Please make a contribution today.

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John Brigande provides commentary: Hearing in the mouse of Usher

Oregon Health & Science University

The March issue of Nature Biotechnology brings together a set of articles that provide an overview of promising RNA-based therapies and the challenges of clinical validation and commercialization. In his News and Views essay, “Hearing in the mouse of Usher,” John V. Brigande, Ph.D., provides commentary on two studies in the issue that report important progress in research on gene therapy for the inner ear.

One in eight people in the United States aged 12 years or older has hearing loss in both ears. That figure suggests that, if you don’t have hearing loss, you likely know someone who does. Worldwide, hearing loss profoundly interferes with life tasks like learning and interpersonal communication for an estimated 32 million children and 328 million adults worldwide. Inherited genetic mutations cause about 50 percent of these cases.

The challenge in developing gene therapy for the inner ear isn’t a lack of known genes associated with hearing loss, but a lack of vectors to deliver DNA into cells. Brigande, associate professor of otolaryngology and cell, developmental, and cancer biology at the OHSU School of Medicine, provides perspective on companion studies that demonstrate adeno-associated viral vectors as a potent gene transfer agent for cochlear cell targets.

The first study demonstrates safe and efficient gene transfer to hair cells of the mouse inner ear using a synthetic adeno-associated viral vector that promises to be a powerful starting point for developing appropriate vectors for use in the human inner ear. The second study demonstrates that a single neonatal treatment with this viral vector successfully delivers a healthy gene to the inner ear to achieve unprecedented recovery of hearing and balance in a mouse model of a disease called Usher syndrome. Individuals with Usher syndrome type 1c are born deaf and with profound balance issues and experience vision loss by early adolescence. The research teams were led by scientists from the Harvard School of Medicine.

Brigande sees these new studies as potentially spurring investment and kickstarting the development of new approaches to correct a diverse set of deafness genes. 

Hearing Restoration Project consortium member John V. Brigande, Ph.D., is a developmental neurobiologist at the Oregon Hearing Research Center. He also teaches in the Neuroscience Graduate Program and in the Program in Molecular and Cellular Biology at the Oregon Health & Science University. This blog was reposted with the permission of Oregon Health & Science University.

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The HRP Shifts Gears for Greater Impact

By Peter Barr-Gillespie, Ph.D.

It’s remarkable to me that the Hearing Restoration Project (HRP) is five years old! While the past five years revealed that regeneration of sensory hair cells is more complex than anticipated, our scientists have nonetheless made significant progress. Several notable HRP research projects supported by Hearing Health Foundation (HHF) were published in 2016, and more are on the way.

Financial investment in the HRP is crucial for our success. Through the HRP, HHF supports promising innovative research areas that due to the lack of available funds are not adequately financed by other agencies. We continue to acquire large-scale genomics datasets, and the more we generate the more valuable they all are—comparing the results from different types of experiments is a key approach of the HRP.

In 2017 we will see a change in the way the HRP conducts its research. At our HRP meeting this past November, the consortium updated its research methods for the upcoming year, choosing to focus and devote more resources on two promising, major experimental strategies. This is a shift from the approach over the past five years, when the HRP followed various independent paths to understanding hair cell regeneration.

The first project will use “single-cell sequencing” experiments, which will reveal the molecular processes of hair cell regeneration in chicks and fish with unprecedented resolution. Single-cell methods allow us to examine thousands of genes in hundreds of individually isolated supporting cells, some of which are responding to hair cell damage.

With these voluminous datasets, we will then describe the succession of molecular changes needed to regenerate hair cells. Results from these experiments will be compared with similar experiments examining hair cell damage in mice, which like all mammals, including humans, do not regenerate hair cells.

The second project will examine whether epigenetic DNA modification (the inactivation of genes by chemical changes to the DNA) is why mice supporting cells are unable to transform into hair cells after damage to the ear. Our existing data suggests this is the case, and so a strategy for hearing restoration may involve the reversal of these epigenetic modifications.

The first project will allow us to identify the genes involved, and the second project will help us understand how to effectively manipulate those genes despite their DNA modifications—and to biologically restore hearing.

The consortium approach funded by HHF provides a unique opportunity; the collaboration of 15 outstanding hearing investigators will lead to results far more quickly than traditional projects that rely on a single investigator. All HRP investigators plan projects and interpret data arising from them, allowing us to collectively utilize our 200-plus years of experience we have studying the ear.

HHF has been able to increase HRP funding for 2017 compared with 2016—for this I am grateful. However, there are several research needs unmet. Increased funding levels would speed our deeper understanding of hair cell regeneration, which will ultimately lead us to find therapies to treat human hearing loss and tinnitus.

Most of all, we are looking to add additional scientists to HRP labs to increase productivity and significantly accelerate research progress. There is also an urgent need for more “bioinformatics” scientists to thoroughly examine our data and identify common threads buried deep within our results. In addition, the HRP has research projects that have been placed on hold until funding is found for them.

We are excited about the coming year’s planned research, and eagerly await the results. On behalf of myself and the other scientists who make up the HRP, I thank you for your investment and interest in our work. I look forward to giving you further updates.

HRP scientific director Peter Barr-Gillespie, Ph.D., is the associate vice president for Basic Research and a professor of otolaryngology at the Oregon Hearing Research Center, and a senior scientist at the Vollum Institute, all at Oregon Health & Science University. 

We need your help in funding the exciting work of hearing and balance scientists.

To donate today to support HHF's groundbreaking research,

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New Insights Into Age-Related Hearing Loss

By Ruili Xie, Ph.D.

Age-related hearing loss (ARHL), also known as presbycusis, is one of the most prevalent health conditions affecting older adults. The leading cause of ARHL is generally attributed to damage in the ear during aging, which include the loss of the inner ear’s sensory hair cells and spiral ganglion cells (SGCs).  

Hair cells act like antennae for the auditory system to receive sound information from the environment. SGCs are the nerve cells that connect the ear and the brain, with their peripheral branches receiving sound information from hair cells, and their central branches forming the auditory nerve to pass information to the brain. Recent studies showed that the terminals (endpoints) of SGC peripheral branches are vulnerable and can be damaged during aging, which are thought to be the primary cause of ARHL.    

However, the majority (over 70 percent) of SGC peripheral terminals survive normal aging. It is unclear whether, with age, sound information is reliably transmitted through the surviving SGCs to the brain; and if not, how this may contribute to ARHL.

One particular point of interest lies in the terminals of the SGC central branches (the auditory nerve synapses) that activate their target neurons in the brain. Deterioration in the information flow at these synapses with age would reduce sensory input to the brain and lead to ARHL.

For the first time, Dr. Paul B. Manis and I have found that the transmission of information from SGCs to their target neurons in the cochlear nucleus (the first auditory station in the brain) is compromised in aged mice with ARHL. The transmission process deteriorates due to abnormal calcium signaling at the central terminals of the SGCs. The study not only proposes a novel brain mechanism that underlies ARHL, but also provides new strategies in developing future clinical treatments.


Ruili Xie, Ph.D., a 2009 and 2010 Emerging Research Grants recipient, is an assistant professor in the Department of Neuroscience at the University of Toledo, in Ohio.The study “Synaptic Transmission at the Endbulb of Held Deteriorates During Age-Related Hearing Loss” appeared in The Journal of Physiology on Sept. 13, 2016.

We need your help supporting innovative hearing and balance science through our Emerging Research Grants program. Please make a contribution today.

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Hearing Beyond the Hair Cell

By Yehoash Raphael, Ph.D.

Recently, it became clear that loud signals can also damage the connecting interface between the hair cell and the auditory nerve. This interface is the synapse. When the synapse is disrupted, hearing is impaired even without the loss of hair cells, leading to a condition called synaptopathy.

Experiments using transgenic mice showed that elevating levels of a specific molecule called NT3 in the area of the synapse can heal synaptopathy caused by exposure to loud noise. Since transgenic technology is a research tool not applicable for clinical use on humans, it is now necessary to design methods for elevating NT3 in human ears, leading to repair of synaptopathy. This is an important task, because if left untreated, synaptopathy progresses to include nerve cell death and permanent hearing deficits.

One potential way to increase NT3 concentration in the cochlea is by the use of gene transfer technology, which is based on infecting cochlear cells with viruses that are engineered to secrete NT3 and not cause infections. A potential risk of this method is that the site of NT3 is not restricted to the area of the synapses affected by the synaptopathy; NT3 can influence other types of cells.

In my lab at the University of Michigan, we tested the outcome of injecting such viruses on the structure and function of normal (intact) ears. We determined that the procedure resulted in the deterioration of hearing thresholds, and the auditory nerve and its connectivity to the hair cells were also negatively affected.

This negative outcome indicates that treatment of synaptopathy should be based on a more specific way to provide NT3 in an area restricted to the synaptic region. My work with the Hearing Restoration Project is dedicated to optimization of gene transfer technology in the cochlea, and may assist in finding more detailed methods for NT3 gene transfer that better target affected cells.

More information on Dr. Raphael’s research can be found in his report, “Viral-mediated Ntf3 overexpression disrupts innervation and hearing in nondeafened guinea pig cochleae,” published in the journal Molecular Therapy—Methods & Clinical Development on August 3, 2016.

Yehoash Raphael, Ph.D., is the The R. Jamison and Betty Williams Professor at the Kresge Hearing Research Institute, in the Department of Otolaryngology–Head and Neck Surgery at the University of Michigan.

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New Player Identified in Hair Cell Development

By Betty Zou, Sunnybrook Research Institute

Sensory hair cells (red) and supporting cells (green) are intricately organized in the developed cochlea. Supporting cells have high levels of the Kremen1 protein, which is stained with a green fluorescent marker here. [Image courtesy of Dr. Alain Dabdoub]

Sensory hair cells (red) and supporting cells (green) are intricately organized in the developed cochlea. Supporting cells have high levels of the Kremen1 protein, which is stained with a green fluorescent marker here. [Image courtesy of Dr. Alain Dabdoub]

There are roughly 37.2 trillion cells in the human body, each of which can be categorized into one of about 200 different types. What’s remarkable about this immense number and diversity of cells is that they all came from a microscopic cluster that comprises the embryo. Many of these early progenitor cells start out the same, but they receive different programming instructions along the way that enable them to replicate and differentiate to form various tissues and organs.

Signalling pathways are cellular communication systems that govern whether a cell keeps dividing or stops, where it goes and, ultimately, what it becomes. One such pathway is Wnt (pronounced “wint”) signalling, a group of signal transmission networks that play a critical role in embryonic development. Dr. Alain Dabdoub, a scientist in Biological Sciences at Sunnybrook Research Institute, is studying how Wnt signalling affects inner ear development and hearing. A new study by his team has shown for the first time that Kremen1, a poorly understood member of the Wnt network, plays a direct role in the formation of the cochlea, a spiral-shaped auditory sensory organ in the inner ear.

“We know that initially at the very early stages [of development], Wnt signalling pushes cells to proliferate,” says Dabdoub. “Then division stops and cell differentiation occurs. We’re trying to find out what promotes this high level of Wnt and also what decreases it.”

Kremen1 is a protein that sits on the cell surface where it receives and transmits signals to the cellular machinery inside. Previous studies have shown that it blocks Wnt signalling, so Dabdoub and his team decided to investigate whether Kremen1 is involved in cell differentiation in the cochlea.

The researchers found that at an early embryonic stage Kremen1 was present in the precursor cells that give rise to hair cells and supporting cells. Shortly thereafter, Kremen1 was only found in the supporting cells that surround hair cells. When the researchers forced the precursor cells to overproduce Kremen1, fewer of them went on to become hair cells and more became supporting cells. In contrast, knocking down levels of Kremen1 resulted in more hair cells. The results were published in August 2016 in the journal Scientific Reports.

The cochlea contains tens of thousands of hair cells, which have hair bundles on their surface to detect and amplify sound. In mammals, when these cells are damaged or destroyed, they are not replaced and hearing loss results. Supporting cells, on the other hand, remain abundant during an individual’s lifetime and do not appear to be affected by the insults that batter hair cells.

Dabdoub’s research seeks to understand how the cochlea and hair cells form, as well as how these sensory cells can be replenished to restore hearing. “If you think about regeneration, where are the cells that you’re going to regenerate coming from?” he says.

The survival of supporting cells makes them excellent candidates from which to regrow hair cells, but they must first replicate to ensure there are enough to maintain a stable number of supporting cells and form new hair cells. Dabdoub thinks that exploiting the proliferation-enhancing properties of Wnt signalling will help achieve this. His finding that Kremen1 plays an important role in cell fate decisions in the cochlea will be critical to future efforts to regenerate hair cells. “This is a molecule that we should keep an eye on as we work towards regeneration,” he says.

Funding for this study came from the Hearing Health Foundation’s Hearing Restoration Project, Koerner Foundation and Sunnybrook Hearing Regeneration Initiative.

This blog was reposted with the permission of Sunnybrook Research Institute.

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To donate today to support HHF's groundbreaking research,

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Noise-Induced Brain Inflammation May Result in Painful Hearing

By Drs. Senthilvelan Manohar, Kelly Radziwon, and Richard Salvi

What do jet engines, sirens, and rock bands have in common? The sounds they emit are so intense that they are not only loud, but also painful, sometimes evoking a painful sensation around the external ear. The acoustic threshold for pain, 130-140 dB SPL, is intense enough to destroy or damage the delicate sensory hair cells, supporting cells and auditory nerve fibers in the inner ear. The axons from the auditory nerve deliver their messages to neurons located in the cochlear nuclei in the brainstem. 

In a recent paper published in Molecular and Cellular Neuroscience, Drs. Baizer and Manohar at the University at Buffalo were surprised to find that intense noise exposures that destroyed the sensory hair cells in the rat inner ear led to a prolonged period of auditory nerve fiber degeneration in the cochlear nucleus in the brainstem (Bazier et al., Neuroscience 303 (2015) 299–311). Nerve fiber degeneration was still occurring 6-9 months post-exposure, nearly a third of the rat’s lifespan. In brain regions where the fibers were degenerating, there was robust upregulation of brain immune cells (microglia), indicative of long-term neuro-inflammation triggered by the release of inflammatory molecules in the brain. Since sensory nerve fibers (e.g., pain, touch) from the face, head, neck and shoulders (facial, trigeminal and spinal nerves) enter the cochlear nucleus, the long-term neuro-inflammation occurring in this region could lower pain thresholds (hyperalgesia). If this were to occur, much lower, moderate-intensity sounds (60-80 dB) might be sufficient to cause hyperacusis (loudness intolerance) with ear pain.


With funding from the Hearing Health Foundation obtained by Drs. Radziwon* and Manohar to identify pain-related molecules in the auditory pathway as a result of noise exposure, Drs. Manohar, Adler, and Salvi carried out a second study in which they measured noise-induced changes in the expression (amount) of genes involved in the synthesis of proteins known to be involved in neuropathic pain and neuro- inflammation. Interestingly, the researchers found that intense noise exposure significantly altered the expression of six genes (Ccl12, Tlr2, Oprd1, II1b, Ntrk1 & Kcnq3) in the cochlear nucleus (Manohar et al., Molecular and Cellular Neuroscience 75 (2016) 101–112). These results suggest that noise-induced inflammation in the parts of the central auditory pathway that also processes sensory information related to pain might, in turn, activate the central pain pathway thus producing ear pain. Determining whether neuro-inflammation is directly responsible for ear pain will open the door for novel interventions to treat hearing loss and hyperacusis.

*Kelly Radziwon, Ph.D., is a 2015 Emerging Research Grants recipient. Her grant was generously funded by Hyperacusis Research Ltd. Learn more about Radziwon and her work in “Meet the Researcher.”

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Enjoy Summer Concert Season Right

By the Better Hearing Institute

With at least another month-and-a-half left of summer concert season, we thought it would be a good time to remind music lovers to pack the earplugs. It’s an easy and smart way to make sure you can enjoy those tunes for years to come.

Bringing earplugs to that next concert is more than a good idea, it should be a must, says the Better Hearing Institute (BHI). Millennials and teens especially should think twice about music volume because data show that hearing loss is on the rise in these age groups, which means they’re permanently losing some of their hearing at younger ages.

But take heart. Earplugs really can help. One study, carried out in conjunction with an outdoor music festival in Amsterdam last fall, found that festival-goers who wore earplugs were roughly five times less likely to have some temporary hearing loss than those who didn’t wear them. The earplug-users also were less likely to suffer from tinnitus afterwards.

Any sounds at or above 85 dBA for a prolonged period of time can be unsafe. The sounds at that Dutch music festival were at 100 decibels, pretty consistently, for 4-and-a-half hours. At that sound level, hearing damage can occur in just 15 minutes.

Luckily, earplugs are pretty easy to come by. Disposable earplugs, made of foam or silicone, usually can be found at local pharmacies. They’re practical because you can still hear music and conversation when they’re in your ears. But when they fit snuggly, they’re effective in adequately blocking out dangerously loud sounds.

The impact of noise on our ears

We hear sound when delicate hair cells in our inner ear vibrate, creating nerve signals that the brain understands as sound. But just as we can overload an electrical circuit, we also can overload these vibrating hair cells. Loud noise damages these delicate hair cells, resulting in sensorineural hearing loss and often tinnitus (ringing in the ears). The cells that are the first to be damaged or die are those that vibrate most quickly—those that allow us to hear higher-frequency sounds clearly.

Warning signs of too much noise

If you have to shout over the noise to be heard by someone within arm’s length, the noise is probably in the dangerous range. Here are the warning signs:

  • You have pain in your ears after leaving a noisy area.

  • You hear ringing or buzzing (tinnitus) in your ears immediately after exposure to noise.

  • You suddenly have difficulty understanding speech after exposure to noise; you can hear people talking but can’t understand them.

Repeated exposure to loud noise, over an extended period of time, presents serious risks to hearing health.

The content for this blog post originated in a press release issued by The Better Hearing Institute on July 19, 2016.

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