New Research on Noise-Induced Tinnitus

The Hearing Review recently highlighted new research conducted at the University of Pittsburgh School of Medicine that identified a cause for noise-induced tinnitus and a drug that prevents its onset. Thanos Tzounopoulos, Ph.D., led a research team that used the FDA approved epilepsy drug retigabine to prevent the onset of tinnitus in mice following exposure to loud noise. 

Dr. Tzounopoulos and his team focused their research on a particular area of the brain where mechanisms involved in producing "phantom" sounds are known to reside- the dorsal cochlear nucleus (DCN). The Hearing Review depicts the research methodology the following way:

From previous research in a mouse model, [Dr. Tzounopoulos and his team] knew that tinnitus is associated with hyperactivity of DCN cells, which fire impulses even when there is no actual sound to perceive. For the new experiments, they took a close look at the biophysical properties of tiny channels, called KCNQ channels... 

“We found that mice with tinnitus have hyperactive DCN cells because of a reduction in KCNQ potassium channel activity,” Tzounopoulos said. “These KCNQ channels act as effective ‘brakes’ that reduce excitability or activity of neuronal cells.” 

Tzounopoulos and his team tested whether an FDA-approved epilepsy drug called retigabine, which specifically enhances KCNQ channel activity, could prevent the development of tinnitus. 

The researchers found that mice that were treated with retigabine immediately after noise exposure did not develop tinnitus. “This is an important finding that links the biophysical properties of a potassium channel with the perception of a phantom sound,” Tzounopoulos said. “Tinnitus is a channelopathy, and these KCNQ channels represent a novel target for developing drugs that block the induction of tinnitus in humans.” 

This research offers hope for a potential medicine that could prevent noise-induced tinnitus! 

For more information on this research and the source of this article, click here.


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