ArticleThe Journal of physiology2008
Initial segment Kv2.2 channels mediate a slow delayed rectifier and maintain high frequency action potential firing in medial nucleus of the trapezoid body neurons.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
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Who cites it
79 citing papers in PubMed.
- Article
- Biophysical properties of the membrane influence spike initiation dynamics and neuronal excitability: a focus on Kv1 channels in myelinated axons.Proceedings. Biological sciences · 2025Review
- Article
- Molecular logic for cellular specializations that initiate the auditory parallel processing pathways.Nature communications · 2025Article
- Mechanistic insights regarding neuropsychiatric and neuropathologic impacts of air pollution.Critical reviews in toxicology · 2024Review
- Molecular logic for cellular specializations that initiate the auditory parallel processing pathways.bioRxiv : the preprint server for biology · 2024Article
- Mono-allelic KCNB2 variants lead to a neurodevelopmental syndrome caused by altered channel inactivation.American journal of human genetics · 2024Article
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KThe Journal of comparative neurology · 2024Article
- Glucocorticoids modulate neural activity via a rapid non-genomic effect on Kv2.2 channels in the central nervous system.Neurobiology of stress · 2024Article
- Kv2 channels contribute to neuronal activity within the vagal afferent-nTS reflex arc.American journal of physiology. Cell physiology · 2024Article
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KbioRxiv : the preprint server for biology · 2023Article
- Modulation of potassium conductances optimizes fidelity of auditory information.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Protein Kinase C Controls the Excitability of Cortical Pyramidal Neurons by Regulating Kv2.2 Channel Activity.Neuroscience bulletin · 2022Article
- Article
- Location, location, location: the organization and roles of potassium channels in mammalian motoneurons.The Journal of physiology · 2021Article
- Modulation of Neuronal Potassium Channels During Auditory Processing.Frontiers in neuroscience · 2021Review
- Cytoskeletal and synaptic polarity of LWamide-like+ ganglion neurons in the sea anemoneThe Journal of experimental biology · 2020Article
- Article
- Molecular determinants of afferent sensitization in a rat model of cystitis with urothelial barrier dysfunction.Journal of neurophysiology · 2019Article
- A molecular rheostat: Kv2.1 currents maintain or suppress repetitive firing in motoneurons.The Journal of physiology · 2019Article
19 more citing papers are in PubMed but not listed here.
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6 authors.
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Abstract
The medial nucleus of the trapezoid body (MNTB) is specialized for high frequency firing by expression of Kv3 channels, which minimize action potential (AP) duration, and Kv1 channels, which suppress multiple AP firing, during each calyceal giant EPSC. However, the outward K(+) current in MNTB neurons is dominated by another unidentified delayed rectifier. It has slow kinetics and a peak conductance of approximately 37 nS; it is half-activated at -9.2 +/- 2.1 mV and half-inactivated at -35.9 +/- 1.5 mV. It is blocked by several non-specific potassium channel antagonists including quinine (100 microm) and high concentrations of extracellular tetraethylammonium (TEA; IC(50) = 11.8 mM), but no specific antagonists were found. These characteristics are similar to recombinant Kv2-mediated currents. Quantitative RT-PCR showed that Kv2.2 mRNA was much more prevalent than Kv2.1 in the MNTB. A Kv2.2 antibody showed specific staining and Western blots confirmed that it recognized a protein approximately 110 kDa which was absent in brainstem tissue from a Kv2.2 knockout mouse. Confocal imaging showed that Kv2.2 was highly expressed in axon initial segments of MNTB neurons. In the absence of a specific antagonist, Hodgkin-Huxley modelling of voltage-gated conductances showed that Kv2.2 has a minor role during single APs (due to its slow activation) but assists recovery of voltage-gated sodium channels (Nav) from inactivation by hyperpolarizing interspike potentials during repetitive AP firing. Current-clamp recordings during high frequency firing and characterization of Nav inactivation confirmed this hypothesis. We conclude that Kv2.2-containing channels have a distinctive initial segment location and crucial function in maintaining AP amplitude by regulating the interspike potential during high frequency firing.
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