ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Calcineurin Dysregulation Underlies Spinal Cord Injury-Induced K
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 22 citations in OpenAlex.
- Structural insights into the function, dysfunction and modulation of Kv3 channels.Neuropharmacology · 2025Review
- Molecular mechanism governing the plasticity of use-dependent spike broadening in dorsal root ganglion neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Article
- Individuals With Prior Chronic Pain and Long-Term Opioid Treatment May Experience Persistence of That Pain Even After Subsequent Complete Cervical Spinal Cord Injury: Suggestions From a Prospective Case-Controlled Study.Archives of rehabilitation research and clinical translation · 2024Article
- Progress in treatment of pathological neuropathic pain after spinal cord injury.Frontiers in neurology · 2024Review
- Olfactory ensheathing cells and neuropathic pain.Frontiers in cell and developmental biology · 2023Review
- Glutamine Maintains Satellite Glial Cells Growth and Survival in Culture.Neurochemical research · 2022Article
- Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.Cellular and molecular neurobiology · 2020Review
- KFrontiers in cellular neuroscience · 2020Review
- [Effect of cinobufagin on transient outward potassium current in dorsal root ganglion cells of rats with cancer-induced bone pain].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2019Article
- Nociceptor Signalling through ion Channel Regulation via GPCRs.International journal of molecular sciences · 2019Review
- A novel primary culture method for high-purity satellite glial cells derived from rat dorsal root ganglion.Neural regeneration research · 2019Article
- Regulation of Nociceptive Glutamatergic Signaling by Presynaptic Kv3.4 Channels in the Rat Spinal Dorsal Horn.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- A-Type KFrontiers in molecular neuroscience · 2018Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
Abstract
Dysfunction of the fast-inactivating Kv3.4 potassium current in dorsal root ganglion (DRG) neurons contributes to the hyperexcitability associated with persistent pain induced by spinal cord injury (SCI). However, the underlying mechanism is not known. In light of our previous work demonstrating modulation of the Kv3.4 channel by phosphorylation, we investigated the role of the phosphatase calcineurin (CaN) using electrophysiological, molecular, and imaging approaches in adult female Sprague Dawley rats. Pharmacological inhibition of CaN in small-diameter DRG neurons slowed repolarization of the somatic action potential (AP) and attenuated the Kv3.4 current. Attenuated Kv3.4 currents also exhibited slowed inactivation. We observed similar effects on the recombinant Kv3.4 channel heterologously expressed in Chinese hamster ovary cells, supporting our findings in DRG neurons. Elucidating the molecular basis of these effects, mutation of four previously characterized serines within the Kv3.4 N-terminal inactivation domain eliminated the effects of CaN inhibition on the Kv3.4 current. SCI similarly induced concurrent Kv3.4 current attenuation and slowing of inactivation. Although there was little change in CaN expression and localization after injury, SCI induced upregulation of the native regulator of CaN 1 (RCAN1) in the DRG at the transcript and protein levels. Consistent with CaN inhibition resulting from RCAN1 upregulation, overexpression of RCAN1 in naive DRG neurons recapitulated the effects of pharmacological CaN inhibition on the Kv3.4 current and the AP. Overall, these results demonstrate a novel regulatory pathway that links CaN, RCAN1, and Kv3.4 in DRG neurons. Dysregulation of this pathway might underlie a peripheral mechanism of pain sensitization induced by SCI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.