ArticlePain2016
Adenosine-A1 receptor agonist induced hyperalgesic priming type II.
Article in Pain, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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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.
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Who cites it
23 citing papers in PubMed, 30 citations in OpenAlex.
- The Agonist of Adenosine A1 Receptor Induced Desensitization of delta Opioid receptor-mediated Raf-1/MEK/ERK Signaling by Feedback Phosphorylation of Raf-1-Ser289/296/301.Neurochemical research · 2023Article
- Predictive analytics identifies key factors driving hyperalgesic priming of muscle sensory neurons.Frontiers in neuroscience · 2023Article
- A modulator-bound GPCR structure enables allosteric non-opioid analgesia.Nature structural & molecular biology · 2021Article
- Estrogen receptors in pain modulation: cellular signaling.Biology of sex differences · 2021Review
- Opioid-Induced Hyperalgesic Priming in Single Nociceptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Electroacupuncture Regulates Pain Transition Through Inhibiting PKCε and TRPV1 Expression in Dorsal Root Ganglion.Frontiers in neuroscience · 2021Article
- Article
- Recent advances toward understanding the mysteries of the acute to chronic pain transition.Current opinion in physiology · 2019Article
- Role of Nociceptor Toll-like Receptor 4 (TLR4) in Opioid-Induced Hyperalgesia and Hyperalgesic Priming.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Systemic Morphine Produces Dose-dependent Nociceptor-mediated Biphasic Changes in Nociceptive Threshold and Neuroplasticity.Neuroscience · 2019Article
- Mu-opioid Receptor (MOR) Biased Agonists Induce Biphasic Dose-dependent Hyperalgesia and Analgesia, and Hyperalgesic Priming in the Rat.Neuroscience · 2018Article
- Spinal Inhibition of P2XR or p38 Signaling Disrupts Hyperalgesic Priming in Male, but not Female, Mice.Neuroscience · 2018Article
- Article
- Fentanyl Induces Rapid Onset Hyperalgesic Priming: Type I at Peripheral and Type II at Central Nociceptor Terminals.The 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
- Hyperalgesic priming (type II) induced by repeated opioid exposure: maintenance mechanisms.Pain · 2017Article
- SDF1-CXCR4 Signaling Contributes to the Transition from Acute to Chronic Pain State.Molecular neurobiology · 2017Article
- Marked sexual dimorphism in 5-HTNeuroscience · 2017Article
- Sustained Morphine Administration Induces TRPM8-Dependent Cold Hyperalgesia.The journal of pain · 2017Article
- Gi-protein-coupled 5-HT1B/D receptor agonist sumatriptan induces type I hyperalgesic priming.Pain · 2016Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We have recently shown that repeated exposure of the peripheral terminal of the primary afferent nociceptor to the mu-opioid receptor (MOR) agonist DAMGO ([D-Ala, N-Me-Phe, Gly-ol]-enkephalin acetate salt) induces a model of transition to chronic pain that we have termed type II hyperalgesic priming. Similar to type I hyperalgesic priming, there is a markedly prolonged response to subsequent administration of proalgesic cytokines, prototypically prostaglandin E2 (PGE2). However, type II hyperalgesic priming differs from type I in being rapidly induced, protein kinase A (PKA), rather than PKCε dependent, not reversed by a protein translation inhibitor, occurring in female as well as in male rats, and isolectin B4-negative neuron dependent. We report that, as with the repeated injection of a MOR agonist, the repeated administration of an agonist at the A1-adenosine receptor, also a Gi-protein coupled receptor, N-cyclopentyladenosine (CPA), also produces priming similar to DAMGO-induced type II hyperalgesic priming. In this study, we demonstrate that priming induced by repeated exposure to this A1-adenosine receptor agonist shares the same mechanisms, as MOR-agonist induced priming. However, the prolongation of PGE2 hyperalgesia induced by repeated administration of CPA depends on G-protein αi subunit activation, differently from DAMGO-induced type II priming, in which it depends on the β/γ subunit. These data implicate a novel form of Gi-protein signaling pathway in the type II hyperalgesic priming induced by repeated administration of an agonist at A1-adenosine receptor to the peripheral terminal of the nociceptor.
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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.