New York: Looking at the molecular mechanisms behind tinnitus, a condition induced by exposure to loud noise that causes whistling, clicking, roaring and other phantom sounds, researchers have found a possible drug therapy for this chronic and sometimes debilitating condition.
The study results build on previous research in mouse models demonstrating that tinnitus is associated with hyperactivity of dorsal cochlear nucleus (DCN) cells, which fire impulses even when there is no actual sound to perceive.
The team's work showed that this hyperactivity is caused by a reduction in tiny channels, called KCNQ channels, through which potassium ions travel in and out of the cell.
Based on this finding, KCNQ channel activators have emerged as clinical candidates for preventing the development of tinnitus.
"However, a significant percentage of people are exposed to loud sounds and never develop tinnitus, and there was little known about why that is. That is what we set out to examine in this study," said one of the researchers Thanos Tzounopoulos, associate professor at University of Pittsburgh School of Medicine.
The research was conducted on mice. The researchers found that resilience to tinnitus was linked to reduced activity of KCNQ channel.
The investigators believe a combination of drugs that enhance KCNQ channel activity and reduce activity of another called hyperpolarisation-activated cyclic nucleotide-gated (HCN) channel could promote resilience and reduce susceptibility to tinnitus.
The findings were published online in the journal eLife.