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      Could ‘chemical earmuffs’ prevent noise-induced hearing damage?

      Researchers in the US have identified molecules in the inner ear that are involved in the damage that loud noise causes to hearing. Blocking their activity protected against this damage when mice were exposed to loud noise. These findings could form the basis of new treatments to protect people’s hearing from noise.

      By: Tracey Pollard | 16 March 2020

      Loud noise is a major cause of hearing damage – not only for those who routinely work in noisy places like factories, building sites or nightclubs, but the WHO estimates that over a billion young people are also risking their hearing through listening to music too loud through their headphones.

      How does noise damage hearing?

      Noise damages hearing in two main ways – if it’s really loud, it damages the sound-sensing cells in the inner ear, the hair cells. When hair cells die, they can’t be replaced, and this causes permanent hearing loss. But even noise that’s not so loud can damage hearing in a more subtle way, sometimes called ‘hidden hearing loss’. This kind of damage doesn’t affect hearing thresholds, but instead makes it more difficult to listen when there’s a lot of background noise.

      In this situation, it’s thought that the hair cells themselves aren’t damaged, but instead the connections between the hair cells and auditory nerve cells, which send sound information to the brain, are broken. These connections are called ‘synapses’, and they’re damaged by a process called ‘excitotoxicity’ – this happens when hair cells become over-activated by sound that is too loud.

      A chemical called glutamate damages synapses

      Hair cells release a chemical called glutamate when they detect a sound – the louder the sound, the more glutamate they produce. Glutamate crosses a small gap between the hair cell and an auditory nerve cell (this is the synapse) and binds to a protein on the nerve cell called a ‘receptor’. This triggers the nerve cell to generate an electrical signal and transmit it to the brain, so we hear sound.

      Hair cells form these synapses with numerous auditory nerve cells, while each nerve cell only forms a synapse with one hair cell. The different nerve cells connected to each hair cell signal in response to sounds with different loudnesses – some send signals when the sound is quiet, while others signal when the sound is loud. This allows the brain to receive information about both how loud a sound is, and its pitch (each hair cell detects sound at a particular pitch, and then activates certain nerve cells depending on how loud the sound is).

      If a sound is too loud, the hair cell releases so much glutamate that it floods the synapses and over-stimulates the nerve cells. This breaks the synapses, causing the hair cell to become disconnected from some nerve cells. This means it can no longer send as much information to the brain about the sound it detects. Interestingly, the hair cell can still send information about quiet sounds, but it struggles to send information about louder sounds. As a result, hearing thresholds don’t change, but the ability to listen in noisy environments is affected. The nerve cells that are disconnected are the ones that help to pick out particular sounds from a noisy background – without them, listening in these environments becomes much more difficult.

      Researchers in the US, at the University of Iowa and Washington University in St Louis, have been studying ‘excitotoxicity’ in mice, to understand more about how glutamate damages synapses.

      Blocking specific receptors can prevent glutamate damage

      Different types of receptor can bind glutamate on the surface of an auditory nerve cell. The research team focused on a particular type, which are involved in transmitting sound information to the brain, called AMPA receptors (or AMPARs). These receptors are formed from four smaller protein units, a mixture of units called GluA1, 2, 3 or 4. They showed that AMPARs without any GluA2 were involved in glutamate toxicity, because when they used a drug that could block these receptors specifically, the mice didn’t develop damage to their synapses following exposure to loud noise.

      Crucially, blocking these receptors didn’t stop the mice from hearing (even though AMPARs are needed to hear) – there were enough AMPARs containing GluA2 (that weren’t affected by the drug) to pass on signals to the brain. In effect, the drug acted like chemical earmuffs, protecting the mice from loud noise.

      So what does this mean?

      At the moment, we can’t fix this kind of damage when it occurs. Perhaps preventing the damage from happening in the first place could be a way to protect the hearing of people who are likely to be exposed to loud noise, such as soldiers, factory or construction workers.

      There’s still a way to go before such a drug might be available for use in people. For example, in this study, the researchers had to infuse the drug directly into the inner ear, which wouldn’t be feasible in people – it would require surgery. More research is needed to develop a drug that can be given orally which gets into the inner ear, is effective and safe.

      But for now, this research has provided us with a better understanding of how exactly loud noise damages hearing and has pointed the way towards a possible means to prevent it.

      Find out more

      This research was published earlier last month in the journal PNAS USA, and you can read the abstract on the journal website.

      If you’re interested in finding out more about our research, sign up to receive our Soundbite e-newsletter. It’s a monthly email, filled with the latest news about hearing and tinnitus research.
      Neurons forming synapses
      Neurons forming synapses

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