ArticleNeuroscience letters2010
Spinal NADPH oxidase is a source of superoxide in the development of morphine-induced hyperalgesia and antinociceptive tolerance.
Article in Neuroscience letters, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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
30 citing papers in PubMed, 64 citations in OpenAlex.
- Role of Central Inflammatory and Oxidative Pathways in the Morphine Exacerbation of Cardiovascular Effects of Sepsis in Rats.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Exploring the Role of Bergamot Polyphenols in Alleviating Morphine-Induced Hyperalgesia and Tolerance through Modulation of Mitochondrial SIRT3.Nutrients · 2024Article
- Quercetin Ameliorates Neuropathic Pain after Brachial Plexus AvulsionCurrent neuropharmacology · 2023Article
- Effects of Different Opioid Drugs on Oxidative Status and Proteasome Activity in SH-SY5Y Cells.Molecules (Basel, Switzerland) · 2022Article
- Nox2 contributes to reactive oxygen species-induced redox imbalance in cancer-induced bone pain.American journal of translational research · 2021Article
- Protective Effect of Antioxidants in Nitric Oxide/COX-2 Interaction during Inflammatory Pain: The Role of Nitration.Antioxidants (Basel, Switzerland) · 2020Article
- Natural Antioxidant Control of Neuropathic Pain-Exploring the Role of Mitochondrial SIRT3 Pathway.Antioxidants (Basel, Switzerland) · 2020Article
- Identification of MOR-Positive B Cell as Possible Innovative Biomarker (Mu Lympho-Marker) for Chronic Pain Diagnosis in Patients with Fibromyalgia and Osteoarthritis Diseases.International journal of molecular sciences · 2020Observational
- Reactive oxygen species (ROS) generation is stimulated by κ opioid receptor activation through phosphorylated c-Jun N-terminal kinase and inhibited by p38 mitogen-activated protein kinase (MAPK) activation.The Journal of biological chemistry · 2019Article
- The mitochondrial calcium uniporter contributes to morphine tolerance through pCREB and CPEB1 in rat spinal cord dorsal horn.British journal of anaesthesia · 2019Article
- Allopregnanolone and Progesterone in Experimental Neuropathic Pain: Former and New Insights with a Translational Perspective.Cellular and molecular neurobiology · 2019Review
- Recent development in antihyperalgesic effect of phytochemicals: anti-inflammatory and neuro-modulatory actions.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2018Review
- Resveratrol alleviates inflammatory hyperalgesia by modulation of reactive oxygen species (ROS), antioxidant enzymes and ERK activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- Therapeutic potential of NADPH oxidase 1/4 inhibitors.British journal of pharmacology · 2017Review
- Nitroxidative Signaling Mechanisms in Pathological Pain.Trends in neurosciences · 2016Review
- AMPKα1 knockout enhances nociceptive behaviors and spinal glutamatergic synaptic activities via production of reactive oxygen species in the spinal dorsal horn.Neuroscience · 2016Article
- Pyrrolidine dithiocarbamate inhibits superoxide anion-induced pain and inflammation in the paw skin and spinal cord by targeting NF-κB and oxidative stress.Inflammopharmacology · 2016Article
- SIRT1 protects against myocardial ischemia-reperfusion injury via activating eNOS in diabetic rats.Cardiovascular diabetology · 2015Article
- Review
- The σ1 receptor engages the redox-regulated HINT1 protein to bring opioid analgesia under NMDA receptor negative control.Antioxidants & redox signaling · 2015Article
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
The role of superoxide and its active byproduct peroxynitrite as mediators of nociceptive signaling is emerging. We have recently reported that nitration and inactivation of spinal mitochondrial superoxide dismutase (MnSOD) provides a critical source of these reactive oxygen and nitrogen species during central sensitization associated with the development of morphine-induced hyperalgesia and antinociceptive tolerance. In this study, we demonstrate that activation of spinal NADPH oxidase is another critical source for superoxide generation. Indeed, the development of morphine-induced hyperalgesia and antinociceptive tolerance was associated with increased activation of NADPH oxidase and superoxide release. Co-administration of morphine with systemic delivery of two structurally unrelated NADPH oxidase inhibitors namely apocynin or diphenyleneiodonium (DPI), blocked NADPH oxidase activation and the development of hyperalgesia and antinociceptive tolerance at doses devoid of behavioral side effects. These results suggest that activation of spinal NADPH oxidase contributes to the development of morphine-induced hyperalgesia and antinociceptive tolerance. The role of spinal NADPH oxidase was confirmed by showing that intrathecal delivery of apocynin blocked these events. Our results are the first to implicate the contribution of NADPH oxidase as an enzymatic source of superoxide and thus peroxynitrite in the development of central sensitization associated with morphine-induced hyperalgesia and antinociceptive tolerance. These results continue to support the critical role of these reactive oxygen and nitrogen species in pain while advancing our knowledge of their biomolecular sources.
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