Researchers have discovered the molecular mechanisms responsible for the development of noise-induced tinnitus and possible drug therapy that may reduce the susceptibility to this condition based on their findings. The study was published in the journal eLife.
Previous research had demonstrated that tinnitus is due to hyperactivity of dorsal cochlear nucleus (DCN) cells, which occurs when there is a reduction in KCNQ channels. Researchers from the University of Pittsburgh School of Medicine expanded upon this research and found that for mice who were exposed to loud noise but did not develop tinnitus, KCNQ2/3 channel activity was temporarily reduced. Eventually, activity levels recovered and the hyperpolarization-activated cyclic nucleotide-gated (HCN) channel activity was also reduced.
With these new findings, the research team concluded that a combination of drugs that enhanced KCNQ2/3 channel activity and reduced HCN channel activity could boost resilience to tinnitus and decrease susceptibility. They have already developed novel KCNQ2/3 channel activators and are working on developing HCN channel inhibitors.
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