ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Protection from noise-induced hearing loss by Kv2.2 potassium currents in the central medial olivocochlear system.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 40 citations in OpenAlex.
- Review
- Fast Inhibition Slows and Desynchronizes Mouse Auditory Efferent Neuron Activity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Glucocorticoids modulate neural activity via a rapid non-genomic effect on Kv2.2 channels in the central nervous system.Neurobiology of stress · 2024Article
- Modulation of potassium conductances optimizes fidelity of auditory information.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Experience-dependent flexibility in a molecularly diverse central-to-peripheral auditory feedback system.eLife · 2023Article
- Synaptic plasticity of inhibitory synapses onto medial olivocochlear efferent neurons.The Journal of physiology · 2022Article
- Protein Kinase C Controls the Excitability of Cortical Pyramidal Neurons by Regulating Kv2.2 Channel Activity.Neuroscience bulletin · 2022Article
- Effects of Multisession Anodal Electrical Stimulation of the Auditory Cortex on Temporary Noise-Induced Hearing Loss in the Rat.Frontiers in neuroscience · 2021Article
- Modulation of Neuronal Potassium Channels During Auditory Processing.Frontiers in neuroscience · 2021Review
- In Vitro Wedge Slice Preparation for Mimicking In Vivo Neuronal Circuit Connectivity.Journal of visualized experiments : JoVE · 2020Article
- Synaptic Inhibition of Medial Olivocochlear Efferent Neurons by Neurons of the Medial Nucleus of the Trapezoid Body.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Distinct Distribution Patterns of Potassium Channel Sub-Units in Somato-Dendritic Compartments of Neurons of the Medial Superior Olive.Frontiers in cellular neuroscience · 2019Article
- Your genes decide what you are listening to.Channels (Austin, Tex.) · 2017Article
- Maintenance of neuronal size gradient in MNTB requires sound-evoked activity.Journal of neurophysiology · 2017Article
- Physiology and anatomy of neurons in the medial superior olive of the mouse.Journal of neurophysiology · 2016Article
- Differential Regulation of Action Potential Shape and Burst-Frequency Firing by BK and Kv2 Channels in Substantia Nigra Dopaminergic Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Decreased temporal precision of neuronal signaling as a candidate mechanism of auditory processing disorder.Hearing research · 2015Review
- De novo KCNB1 mutations in infantile epilepsy inhibit repetitive neuronal firing.Scientific reports · 2015Article
- The extracellular matrix molecule brevican is an integral component of the machinery mediating fast synaptic transmission at the calyx of Held.The Journal of physiology · 2015Article
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
The central auditory brainstem provides an efferent projection known as the medial olivocochlear (MOC) system, which regulates the cochlear amplifier and mediates protection on exposure to loud sound. It arises from neurons of the ventral nucleus of the trapezoid body (VNTB), so control of neuronal excitability in this pathway has profound effects on hearing. The VNTB and the medial nucleus of the trapezoid body are the only sites of expression for the Kv2.2 voltage-gated potassium channel in the auditory brainstem, consistent with a specialized function of these channels. In the absence of unambiguous antagonists, we used recombinant and transgenic methods to examine how Kv2.2 contributes to MOC efferent function. Viral gene transfer of dominant-negative Kv2.2 in wild-type mice suppressed outward K(+) currents, increasing action potential (AP) half-width and reducing repetitive firing. Similarly, VNTB neurons from Kv2.2 knock-out mice (Kv2.2KO) also showed increased AP duration. Control experiments established that Kv2.2 was not expressed in the cochlea, so any changes in auditory function in the Kv2.2KO mouse must be of central origin. Further, in vivo recordings of auditory brainstem responses revealed that these Kv2.2KO mice were more susceptible to noise-induced hearing loss. We conclude that Kv2.2 regulates neuronal excitability in these brainstem nuclei by maintaining short APs and enhancing high-frequency firing. This safeguards efferent MOC firing during high-intensity sounds and is crucial in the mediation of protection after auditory overexposure.
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