ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Role of nociceptor αCaMKII in transition from acute to chronic pain (hyperalgesic priming) in male and female rats.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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64 citing papers in PubMed, 83 citations in OpenAlex.
- Article
- Differential Involvement of t-SNARE Proteins and Signaling Pathways During PGE2-Induced TRPV1 Sensitization.Journal of molecular neuroscience : MN · 2026Article
- Incision-triggered neuroimmune remodeling of nociceptor ion channels: from postoperative inflammation to pain chronification.Frontiers in immunology · 2026Review
- GCN2 regulates paclitaxel-induced neuropathic pain.British journal of pharmacology · 2025Article
- The mRNA Translation Inhibitor Vioprolide A Prevents Inflammatory Pain-Like Behaviour With Limited Action on Already Established Pain-Like Behaviour in Mice.European journal of pain (London, England) · 2025Article
- Sex differences in the transition to chronic pain.The Journal of clinical investigation · 2025Review
- Article
- Exploring the role of neutrophils in inflammatory pain hypersensitivity via single-cell transcriptome profiling.Frontiers in immunology · 2025Article
- Exploring the role of spinal astrocytes in the onset of hyperalgesic priming signals in acid-induced chronic muscle pain.PNAS nexus · 2024Article
- Persistent changes in nociceptor translatomes govern hyperalgesic priming in mouse models.bioRxiv : the preprint server for biology · 2024Article
- Satellite glial cells drive the transition from acute to chronic pain in a rat model of hyperalgesic priming.Frontiers in molecular neuroscience · 2023Article
- Predictive analytics identifies key factors driving hyperalgesic priming of muscle sensory neurons.Frontiers in neuroscience · 2023Article
- High-fat diet causes mechanical allodynia in the absence of injury or diabetic pathology.Scientific reports · 2022Article
- SNHG5 knockdown alleviates neuropathic pain induced by chronic constriction injury via sponging miR‑142‑5p and regulating the expression of CAMK2A.Molecular medicine reports · 2022Article
- Calcium Signalling in Breast Cancer Associated Bone Pain.International journal of molecular sciences · 2022Review
- Intercellular Arc Signaling Regulates Vasodilation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Article
- Non-canonical Molecular Targets for Novel Analgesics: Intracellular Calcium and HCN Channels.Current neuropharmacology · 2021Review
- Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion.Frontiers in neuroscience · 2021Article
- Role of GABAAR in the Transition From Acute to Chronic Pain and the Analgesic Effect of Electroacupuncture on Hyperalgesic Priming Model Rats.Frontiers in neuroscience · 2021Article
4 more citing papers are in PubMed but not listed here.
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3 authors at 1 institution in 1 country.
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Abstract
We have previously shown that activation of protein kinase Cε (PKCε) in male rats induces a chronic, long-lasting change in nociceptors such that a subsequent exposure to proinflammatory mediators produces markedly prolonged mechanical hyperalgesia. This neuroplastic change, hyperalgesic priming, is dependent on activation of cytoplasmic polyadenylation element-binding protein (CPEB), downstream of PKCε, and consequent translation of mRNAs in the peripheral terminal of the nociceptor. Since α calmodulin-dependent protein kinase II (αCaMKII), a molecule implicated in neuroplasticity, is a target of CPEB and can also affect CPEB function, we investigated its role in the transition from acute to chronic pain. Priming induced by direct activation of PKCε can be prevented by inhibition of αCaMKII. In addition, direct activation of αCaMKII induces priming, which was not prevented by pretreatment with PKCε antisense, suggesting that αCaMKII is downstream of PKCε in the induction of priming. Activation of ryanodine receptors (RyRs), which can lead to activation of αCaMKII, also induced priming, in a calcium- and αCaMKII-dependent manner. Similarly, inhibition of the RyR and a calcium buffer prevented induction of priming by PKCε. Unlike activation of PKCε, ryanodine and αCaMKII induced priming in female as well as male rats. Our results demonstrate a contribution of αCaMKII to induction of hyperalgesic priming, a phenomenon implicated in the transition from acute to chronic pain.
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