Thanos Tzounopoulos
Pittsburgh Hearing Research Center, University of Pittsburgh
Kv7 (KCNQ) potassium channel plasticity in noise-induced tinnitus and its pharmacological reversal.
Papers (6)
Pathogenic plasticity of Kv7.2/3 channel activity is essential for the induction of tinnitus.
Proceedings of the National Academy of Sciences of the United States of America · 2013
The seminal finding: reduced Kv7.2/3 channel activity in the dorsal cochlear nucleus is essential for tinnitus induction, and reversing it pharmacologically prevents tinnitus in mice.
Noise-induced plasticity of KCNQ2/3 and HCN channels underlies vulnerability and resilience to tinnitus.
eLife · 2015
Why do only some noise-exposed animals get tinnitus? Mice that fail to restore Kv7.2/3 channel activity within about a week develop tinnitus; those that do, become resilient.
Potent KCNQ2/3-specific channel activator suppresses in vivo epileptic activity and prevents the development of tinnitus.
The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
A more potent, more selective KCNQ2/3 activator (SF0034) prevented tinnitus development in mice, and was a safer anticonvulsant than the FDA-approved retigabine.
Transient Delivery of a KCNQ2/3-Specific Channel Activator 1 Week After Noise Trauma Mitigates Noise-Induced Tinnitus.
Journal of the Association for Research in Otolaryngology : JARO · 2021
Even started a week after noise trauma, well after the injury, not just immediately, a specific KCNQ2/3 activator (RL-81) still reduced the development of tinnitus in mice.
Mice with behavioral evidence of tinnitus exhibit dorsal cochlear nucleus hyperactivity because of decreased GABAergic inhibition.
Proceedings of the National Academy of Sciences of the United States of America · 2011
Mice with confirmed behavioral tinnitus show dorsal cochlear nucleus hyperactivity driven by decreased GABAergic inhibition, a precursor finding to the Kv7.2/3 channel work.
Synaptic zinc plasticity shapes adaptive and maladaptive cortical plasticity following cochlear injury.
Science advances · 2026
Synaptic zinc plasticity in auditory cortex drives both the adaptive recovery and the maladaptive hyperactivity that follow cochlear injury.