ArticlePain2018
Isolated nociceptors reveal multiple specializations for generating irregular ongoing activity associated with ongoing pain.
Article in Pain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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Who cites it
51 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.
- Safety and efficacy of intra-articular injection of platelet-rich plasma for the treatment of ankle osteoarthritis: a systematic review and meta-analysis.International orthopaedics · 2023Pooled it
- C-C motif chemokine ligand 12 (CCL12) is a critical chemokine driving postoperative pain.Pain · 2026Article
- Article
- Electrophysiological Properties and Mechanical Sensitivity of Trigeminal Ganglionic Neurons That Innervate the Maxillary Sinus in Mice.International journal of molecular sciences · 2026Article
- The Increased Activity of CaV3.2 Channels Contributes to Nociceptors' Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury in Mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- From nociception in aneural animals to human suffering: toward a comparative biology of pain.The Journal of experimental biology · 2025Review
- Contusive spinal cord injury causes Nav1.8 dysfunction to upregulate small sensory neuron excitability.The Journal of physiology · 2025Article
- Article
- Human sensory neurons exhibit cell-type-specific, pain-associated differences in intrinsic excitability and expression ofbioRxiv : the preprint server for biology · 2025Article
- Maladaptive changes in the homeostasis of AEA-TRPV1/CB1R induces pain-related hyperactivity of nociceptors after spinal cord injury.Cell & bioscience · 2025Article
- Intrinsic adaptive plasticity in mouse and human sensory neurons.The Journal of general physiology · 2025Article
- B cells drive neuropathic pain-related behaviors in mice through IgG-Fc gamma receptor signaling.Science translational medicine · 2024Article
- Mechanism of gabapentinoid potentiation of opioid effects on cyclic AMP signaling in neuropathic pain.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models.bioRxiv : the preprint server for biology · 2024Article
- Induction of long-term hyperexcitability by memory-related cAMP signaling in isolated nociceptor cell bodies.bioRxiv : the preprint server for biology · 2024Article
- Widespread latent hyperactivity of nociceptors outlasts enhanced avoidance behavior following incision injury.bioRxiv : the preprint server for biology · 2024Article
- Peripheral Nervous System Pain Modulation.Current neuropharmacology · 2024Article
- Progress in treatment of pathological neuropathic pain after spinal cord injury.Frontiers in neurology · 2024Review
- Systematic analysis of proximal midgut- and anorectal-originating contractions in larval zebrafish using event feature detection and supervised machine learning algorithms.Neurogastroenterology and motility · 2023Article
- Intrinsic Homeostatic Plasticity in Mouse and Human Sensory Neurons.bioRxiv : the preprint server for biology · 2023Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Ongoing pain has been linked to ongoing activity (OA) in human C-fiber nociceptors, but rodent models of pain-related OA have concentrated on allodynia rather than ongoing pain, and on OA generated in non-nociceptive Aβ fibers rather than C-fiber nociceptors. Little is known about how ongoing pain or nociceptor OA is generated. To define neurophysiological alterations underlying nociceptor OA, we have used isolated dorsal root ganglion neurons that continue to generate OA after removal from animals displaying ongoing pain. We subclassify OA as either spontaneous activity generated solely by alterations intrinsic to the active neuron or as extrinsically driven OA. Both types of OA were implicated previously in nociceptors in vivo and after isolation following spinal cord injury, which produces chronic ongoing pain. Using novel automated algorithms to analyze irregular changes in membrane potential, we have found, in a distinctive, nonaccommodating type of probable nociceptor, induction by spinal cord injury of 3 alterations that promote OA: (1) prolonged depolarization of resting membrane potential, (2) a hyperpolarizing shift in the voltage threshold for action potential generation, and (3) an increase in the incidence of large depolarizing spontaneous fluctuations (DSFs). Can DSFs also be enhanced acutely to promote OA in neurons from uninjured animals? A low dose of serotonin failed to change resting membrane potential but lowered action potential threshold. When combined with artificial depolarization to model inflammation, serotonin also strongly potentiated DSFs and OA. These findings reveal nociceptor specializations for generating OA that may promote ongoing pain in chronic and acute conditions.
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Registered trials
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.