Whether in the disco, on the street or even at work: Many people are regularly surrounded by noise. This can have fatal consequences for your hearing. Researchers are now reporting an active ingredient that could protect against such consequences. This substance blocks certain receptors that are important for the transmission of acoustic stimuli – and apparently cause damage to synapses in the inner ear when exposed to noise. The highlight: by blocking these receptors, noise damage could be prevented at least in mice. Hearing is not impaired by chemical ear protection, as the team explains.
If our hearing gets too much noise, it can suffer permanent damage. This can happen with an extremely loud bang. However, less, but chronic, noise pollution also leads to hearing loss. Doctors distinguish between two forms of noise damage: On the one hand, the high noise levels can destroy the fine hair cells in the inner ear. On the other hand, their contact points with the fibers of the auditory nerve are sometimes also affected – the synapses. At these connection points, the auditory information about the release of the neurotransmitter glutamate is passed on from the inner ear to the auditory nerve. “Excessive release of glutamate can cause noise in the cochlear synapses to cause trauma,” explains scientists led by Ning Hu from the University of Iowa in Iowa City. The constant overstimulation permanently damages the synapses. As a result, in extreme cases, the nerve cells that carry the hearing information to the brain even die.
Protection without damping
But how does it come about? In search of an answer, Hu and his colleagues have now looked at the receptors to which the glutamate binds and exerts its effect. They found that apparently not all receptors are equally involved in the development of so-called synaptopathy. Instead, only a certain class of receptors appears to be responsible for how experiments with mice suggested. These receptors lack a protein subunit called GluA2. In contrast to other glutamate receptors, they are permeable to calcium ions. If the receptors are activated excessively, this could lead to a strong influx of calcium into the neurons in the inner ear – and this could possibly cause the known damage, as the researchers suspect.
How exactly the now identified receptors interfere with the function of the synapses has not yet been conclusively clarified. However, Hu and his team have already found a method to prevent this damage. In the experiment, the scientists specifically blocked the receptors without GluA2 and used an active ingredient called IEM-1460. In fact, it turned out that the administration of this substance meant that the mice did not experience hearing loss when exposed to noise. The drug thus acts as a kind of chemical earmuff. However, this analogy is not entirely correct, as Hus colleague Steven Green emphasizes. The reason: “These earmuffs protect the hearing from damage, but they don’t dampen noise.” How can that be? According to the researchers, the remaining GluA2-containing receptors are sufficient to ensure stimulus transmission. “The mouse still hears well because it still has these receptors,” says Green. “So we have a drug that prevents hearing loss, but not hearing.”
Transferable to humans?
If these results can be transferred to humans, exciting prevention options result. Such a drug could be administered to groups of people who are exposed to a lot of noise in everyday life – for example soldiers on duty or factory workers. Before that happens, however, a few research steps are still necessary. For example, an adjustment of the active ingredient: Up to now, the drug had to be inserted directly into the cochlea during an operation. Hu and his colleagues therefore hope to find a similarly effective agent that can be administered non-invasively. “Our chemical earmuffs are so far only an indication of the direction in which research could go. We do not yet have a proven, effective and safe way of protecting people against noise damage, ”concludes Green.
Source: Ning Hu (University of Iowa, Iowa City) et al., Proceedings of the National Academy of Sciences, doi: 10.1073 / pnas.1914247117