Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus.

Summary

Vulnerability to noise-induced tinnitus is associated with increased spontaneous firing in DCN fusiform cells, driven partly by decreased KCNQ2/3 currents. This study found that noise exposure reduces KCNQ2/3 activity in fusiform cells within 4 days in essentially all exposed mice, but tinnitus only develops in those that fail to compensate for this reduction over the following days. Mice that instead show a re-emergence of KCNQ2/3 activity, along with a reduction in HCN channel activity, develop resilience instead. This highlights KCNQ2/3 and HCN channels as targets for promoting resilience, not just preventing initial injury.

Key findings

• Noise exposure reduces KCNQ2/3 channel activity in DCN fusiform cells within days, in most exposed mice.
• Tinnitus develops specifically in mice that fail to restore this activity within about a week.
• Resilient mice show KCNQ2/3 activity re-emerging alongside reduced HCN channel activity.
• Points to KCNQ2/3 and HCN channels as targets for promoting resilience, not only preventing induction.