ArticleScientific reports2016
Enhanced excitability and suppression of A-type K(+) currents in joint sensory neurons in a murine model of antigen-induced arthritis.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Satellite Glial Cells Control Sensory Neuron Excitability via the Release of Fibulin-2.bioRxiv : the preprint server for biology · 2026Article
- Mast cell-expressed Mrgprb2/MRGPRX2 mediates gout pain and inflammation via a neuroimmune axis.JCI insight · 2026Article
- Sensory neuron-specific block of multifaceted sodium channels mitigates neuropathic pain behaviors of osteoarthritis.Pain reports · 2025Article
- Using in vivo calcium imaging to examine joint neuron spontaneous activity and home cage analysis to monitor activity changes in mouse models of arthritis.Arthritis research & therapy · 2025Article
- Pain Hypersensitivity in SLURP1 and SLURP2 Knock-out Mouse Models of Hereditary Palmoplantar Keratoderma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Skin Reinnervation by Collateral Sprouting Following Spared Nerve Injury in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- mTORC2 mediates structural plasticity in distal nociceptive endings that contributes to pain hypersensitivity following inflammation.The Journal of clinical investigation · 2022Article
- Selective block of sensory neuronal T-type/Cav3.2 activity mitigates neuropathic pain behavior in a rat model of osteoarthritis pain.Arthritis research & therapy · 2022Article
- Subcellular localization of neuronal nuclei (NeuN) antigen in size and calcitonin gene-related peptide (CGRP) populations of dorsal root ganglion (DRG) neurons during acute peripheral inflammation.Neuroscience letters · 2021Article
- The neuronal potassium current IPhysiological reports · 2021Article
- Kv4.3 Channel Dysfunction Contributes to Trigeminal Neuropathic Pain Manifested with Orofacial Cold Hypersensitivity in Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- The Input-Output Relation of Primary Nociceptive Neurons is Determined by the Morphology of the Peripheral Nociceptive Terminals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Characteristics of voltage-gated potassium currents in monosodium urate induced gouty arthritis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2020Article
- Understanding the Molecular Mechanisms Underlying the Pathogenesis of Arthritis Pain Using Animal Models.International journal of molecular sciences · 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
- The Secretomes of Painful Versus Nonpainful Human Schwannomatosis Tumor Cells Differentially Influence Sensory Neuron Gene Expression and Sensitivity.Scientific reports · 2019Article
- Neuronal FcγRI mediates acute and chronic joint pain.The Journal of clinical investigation · 2019Article
- The Role of Kv7/M Potassium Channels in Controlling Ectopic Firing in Nociceptors.Frontiers in molecular neuroscience · 2017Article
- Peripheral mechanisms of arthritic pain: A proposal to leverage large animals forNeurobiology of pain (Cambridge, Mass.)Review
- Down-regulation of Kv4.3 channels and a-type KMolecular painArticle
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Pain is a dominant symptom of rheumatoid arthritis (RA) and its adequate treatment represents a major unmet need. However, the cellular mechanisms that drive arthritis pain are largely unexplored. Here, we examined the changes in the activity of joint sensory neurons and the associated ionic mechanisms using an animal model of antigen-induced arthritis (AIA). Methylated-bovine serum albumin (mBSA), but not vehicle challenge, in the ankle of previously immunized mice produced time-dependent symptoms of arthritis, including joint inflammation, primary mechanical hyperalgesia in the ipsilateral ankle, and secondary mechanical and heat hyperalgesia in the ipsilateral hindpaw. In vivo electrophysiological recordings revealed that Dil-labeled joint sensory neurons in AIA mice exhibited a greater incidence of spontaneous activity, mechanically evoked after-discharges, and/or increased responses to mechanical stimulation of their receptive fields, compared to control animals. Whole-cell recordings in vitro showed that AIA enhanced the excitability of joint sensory neurons. These signs of neuronal hyperexcitability were associated with a significant reduction in the density of A-type K(+) currents. Thus, our data suggest that neuronal hyperexcitability, brought about in part by reduced A-type K(+) currents, may contribute to pain-related behaviors that accompany antigen-induced arthritis and/or other antigen-mediated diseases.
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