Blast-Induced tinnitus and spontaneous firing changes in the rat dorsal cochlear nucleus

2014 ◽  
Vol 92 (11) ◽  
pp. 1466-1477 ◽  
Author(s):  
Hao Luo ◽  
Edward Pace ◽  
Xueguo Zhang ◽  
Jinsheng Zhang
2015 ◽  
Vol 81 ◽  
pp. 14-19 ◽  
Author(s):  
Tamara Perez-Rosello ◽  
Charles T. Anderson ◽  
Cindy Ling ◽  
Stephen J. Lippard ◽  
Thanos Tzounopoulos

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Shuang Li ◽  
Bopanna I Kalappa ◽  
Thanos Tzounopoulos

Vulnerability to noise-induced tinnitus is associated with increased spontaneous firing rate in dorsal cochlear nucleus principal neurons, fusiform cells. This hyperactivity is caused, at least in part, by decreased Kv7.2/3 (KCNQ2/3) potassium currents. However, the biophysical mechanisms underlying resilience to tinnitus, which is observed in noise-exposed mice that do not develop tinnitus (non-tinnitus mice), remain unknown. Our results show that noise exposure induces, on average, a reduction in KCNQ2/3 channel activity in fusiform cells in noise-exposed mice by 4 days after exposure. Tinnitus is developed in mice that do not compensate for this reduction within the next 3 days. Resilience to tinnitus is developed in mice that show a re-emergence of KCNQ2/3 channel activity and a reduction in HCN channel activity. Our results highlight KCNQ2/3 and HCN channels as potential targets for designing novel therapeutics that may promote resilience to tinnitus.


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