ArticleNeuroscience2009
Activation of Gi induces mechanical hyperalgesia poststress or inflammation.
Article in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
The trial behind it
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Who cites it
28 citing papers in PubMed, 45 citations in OpenAlex.
- AAV-glycine receptor α3 alleviates CFA-induced inflammatory pain by downregulating ERK phosphorylation and proinflammatory cytokine expression in SD rats.Molecular medicine (Cambridge, Mass.) · 2023Article
- Duration of Reduction in Enduring Stress-Induced Hyperalgesia Via FKBP51 Inhibition Depends on Timing of Administration Relative to Traumatic Stress Exposure.The journal of pain · 2022Article
- Age-Dependent Sexual Dimorphism in Susceptibility to Develop Chronic Pain in the Rat.Neuroscience · 2018Article
- An Integrative Neuroscience Framework for the Treatment of Chronic Pain: From Cellular Alterations to Behavior.Frontiers in integrative neuroscience · 2018Article
- A-Kinase Anchoring Protein 79/150 Scaffolds Transient Receptor Potential A 1 Phosphorylation and Sensitization by Metabotropic Glutamate Receptor Activation.Scientific reports · 2017Article
- Regulation of Expression of Hyperalgesic Priming by Estrogen Receptor α in the Rat.The journal of pain · 2017Article
- Gi-protein-coupled 5-HT1B/D receptor agonist sumatriptan induces type I hyperalgesic priming.Pain · 2016Article
- Serotonin Receptor 2B Mediates Mechanical Hyperalgesia by Regulating Transient Receptor Potential Vanilloid 1.Journal of molecular neuroscience : MN · 2016Article
- Article
- Mas-Related Gene (Mrg) C Activation Attenuates Bone Cancer Pain via Modulating Gi and NR2B.PloS one · 2016Article
- Repeated Mu-Opioid Exposure Induces a Novel Form of the Hyperalgesic Priming Model for Transition to Chronic Pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Distinct terminal and cell body mechanisms in the nociceptor mediate hyperalgesic priming.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Accounting for the delay in the transition from acute to chronic pain: axonal and nuclear mechanisms.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- The pharmacology of nociceptor priming.Handbook of experimental pharmacology · 2015Review
- Acidosis Mediates the Switching of Gs-PKA and Gi-PKCε Dependence in Prolonged Hyperalgesia Induced by Inflammation.PloS one · 2015Article
- Commonalities between pain and memory mechanisms and their meaning for understanding chronic pain.Progress in molecular biology and translational science · 2015Review
- Second messengers mediating the expression of neuroplasticity in a model of chronic pain in the rat.The journal of pain · 2014Article
- The fundamental unit of pain is the cell.Pain · 2013Review
- Article
- Protein kinase Cε is required for spinal analgesic synergy between delta opioid and alpha-2A adrenergic receptor agonist pairs.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
In studies of the role of primary afferent nociceptor plasticity in the transition from acute to chronic pain we recently reported that exposure to unpredictable sound stress or a prior inflammatory response induces long-term changes in the second messenger signaling pathway, in nociceptors, mediating inflammatory hyperalgesia; this change involves a switch from a G(s)-cAMP-PKA to a G(i)-PKCepsilon signaling pathway. To more directly study the role of G(i) in mechanical hyperalgesia we evaluated the nociceptive effect of the G(i) activator, mastoparan. Intradermal injection of mastoparan in the rat hind paw induces dose-dependent (0.1 ng-1 microg) mechanical hyperalgesia. The highly selective inhibitors of G(i), pertussis toxin, and of protein kinase C epsilon (PKCepsilon), PKCepsilonV(1-2), both markedly attenuate mastoparan-induced hyperalgesia in stressed rats but had no effect on mastoparan-induced hyperalgesia in unstressed rats. Similar effects were observed, at the site of nociceptive testing, after recovery from carrageenan-induced inflammation. These studies provide further confirmation for a switch to a G(i)-activated and PKCepsilon-dependent signaling pathway in primary mechanical hyperalgesia, induced by stress or inflammation.
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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.