Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus
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...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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eLife Sciences Publications Ltd
2015-08-01
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| Series: | eLife |
| Subjects: | |
| Online Access: | https://elifesciences.org/articles/07242 |
| _version_ | 1811227657636937728 |
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| author | Shuang Li Bopanna I Kalappa Thanos Tzounopoulos |
| author_facet | Shuang Li Bopanna I Kalappa Thanos Tzounopoulos |
| author_sort | Shuang Li |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-04-12T09:45:48Z |
| format | Article |
| id | doaj.art-d2615bc928e34754b163b35f3b0ebbb5 |
| institution | Directory Open Access Journal |
| issn | 2050-084X |
| language | English |
| last_indexed | 2024-04-12T09:45:48Z |
| publishDate | 2015-08-01 |
| publisher | eLife Sciences Publications Ltd |
| record_format | Article |
| series | eLife |
| spelling | doaj.art-d2615bc928e34754b163b35f3b0ebbb52022-12-22T03:37:57ZengeLife Sciences Publications LtdeLife2050-084X2015-08-01410.7554/eLife.07242Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitusShuang Li0Bopanna I Kalappa1Thanos Tzounopoulos2Departments of Otolaryngology and Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, United StatesDepartments of Otolaryngology and Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, United StatesDepartments of Otolaryngology and Neurobiology, University of Pittsburgh School of Medicine, Pittsburgh, United StatesVulnerability 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.https://elifesciences.org/articles/07242potassium channelHCN channelstinnitushomeostatic plasticityhyperexcitability-related disorders |
| spellingShingle | Shuang Li Bopanna I Kalappa Thanos Tzounopoulos Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus eLife potassium channel HCN channels tinnitus homeostatic plasticity hyperexcitability-related disorders |
| title | Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus |
| title_full | Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus |
| title_fullStr | Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus |
| title_full_unstemmed | Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus |
| title_short | Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus |
| title_sort | noise induced plasticity of kcnq2 3 and hcn channels underlies vulnerability and resilience to tinnitus |
| topic | potassium channel HCN channels tinnitus homeostatic plasticity hyperexcitability-related disorders |
| url | https://elifesciences.org/articles/07242 |
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