ArticleNeuroscience2010
Nociceptor subpopulations involved in hyperalgesic priming.
Article in Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 89 citations in OpenAlex.
- Article
- Acetone-Ether-Water Mouse Model of Persistent Itch Fully Resolves Without Latent Pruritic or Cross-Modality Priming.Dermatopathology (Basel, Switzerland) · 2025Article
- Hyperalgesic Priming in the Transition From Acute to Chronic Pain: Focus on Different Models and the Molecular Mechanisms Involved.Journal of pain research · 2025Review
- The Nociceptor Primary Cilium Contributes to Mechanical Nociceptive Threshold and Inflammatory and Neuropathic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Early-life cisplatin exposure induces neuroinflammation and chemotherapy-induced neuropathic pain.Disease models & mechanisms · 2024Article
- Peripheral macrophages contribute to nociceptor priming in mice with chronic intermittent hypoxia.Science signaling · 2024Article
- The Primary Cilium and its Hedgehog Signaling in Nociceptors Contribute to Inflammatory and Neuropathic Pain.Research square · 2024Article
- Neuropathic pain; what we know and what we should do about it.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
- Sensory Neurons, Neuroimmunity, and Pain Modulation by Sex Hormones.Endocrinology · 2021Review
- Interplay of BDNF and GDNF in the Mature Spinal Somatosensory System and Its Potential Therapeutic Relevance.Current neuropharmacology · 2021Review
- Preventing the induction of acid saline-induced fibromyalgia pain in mice by electroacupuncture or APETx2 injection.Acupuncture in medicine : journal of the British Medical Acupuncture Society · 2020Article
- Article
- The mitochondrial calcium uniporter contributes to morphine tolerance through pCREB and CPEB1 in rat spinal cord dorsal horn.British journal of anaesthesia · 2019Article
- Physiologic facet capsule stretch can induce pain & upregulate matrix metalloproteinase-3 in the dorsal root ganglia when preceded by a physiological mechanical or nonpainful chemical exposure.Clinical biomechanics (Bristol, Avon) · 2019Article
- Systemic Morphine Produces Dose-dependent Nociceptor-mediated Biphasic Changes in Nociceptive Threshold and Neuroplasticity.Neuroscience · 2019Article
- Swedish Nerve Growth Factor Mutation (NGFThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Low GRK2 Underlies Hyperalgesic Priming by Glial Cell-Derived Neurotrophic Factor.Frontiers in pharmacology · 2018Article
- Prevention and reversal of latent sensitization of dorsal horn neurons by glial blockers in a model of low back pain in male rats.Journal of neurophysiology · 2017Article
- Marked Sexual Dimorphism in the Role of the Ryanodine Receptor in a Model of Pain Chronification in the Rat.Scientific reports · 2016Article
- Role of Kv4.3 in Vibration-Induced Muscle Pain in the Rat.The journal of pain · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have previously developed a model in the rat for the transition from acute to chronic pain, hyperalgesic priming, in which a long-lasting neuroplastic change in signaling pathways mediates a prolongation of proinflammatory cytokine-induced nociceptor sensitization and mechanical hyperalgesia, induced at the site of a previous inflammatory insult. Induction of priming is mediated by activation of protein kinase C(epsilon) (PKC(epsilon)) in the peripheral terminal of the primary afferent nociceptor. Given that hyperalgesic mediator-induced PKC(epsilon) translocation occurs in isolectin B4 (IB4)(+)-nonpeptidergic but not in receptor tyrosine kinase (TrkA)(+)-peptidergic nociceptors, we tested the hypothesis that hyperalgesic priming was restricted to the IB4(+) subpopulation of nociceptors. After recovery from nerve growth factor (NGF)- and GDNF-induced hyperalgesia, a proinflammatory cytokine, prostaglandin E(2) (PGE(2)) induced, PKC(epsilon)-dependent, markedly prolonged hyperalgesia, two features that define the development of the primed state. Thus, hyperalgesic priming occurs in both the IB4(+)-nonpeptidergic and TrkA(+)-peptidergic subpopulations of nociceptive afferents. Of note, however, while attenuation of PKC(epsilon) prevented NGF-induced priming, the hyperalgesia induced by NGF is PKC(epsilon) independent. We propose that separate intracellular pools of PKC(epsilon), in the peripheral terminals of nociceptors, mediate nociceptor sensitization and the induction of hyperalgesic priming.
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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.