ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Involvement of NOX1/NADPH oxidase in morphine-induced analgesia and tolerance.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 59 citations in OpenAlex.
- Involvement of endolysosome iron in HIV-1 gp120-, morphine-, and iron supplementation-induced disruption of the reactive species interactome and induction of neurotoxicity.Redox report : communications in free radical research · 2025Article
- Therapeutic potential of Bergenin in the management of neurological-based diseases and disorders.Naunyn-Schmiedeberg's archives of pharmacology · 2024Review
- Targeting the Main Sources of Reactive Oxygen Species Production: Possible Therapeutic Implications in Chronic Pain.Current neuropharmacology · 2024Review
- NADPH Oxidases in Pain Processing.Antioxidants (Basel, Switzerland) · 2022Review
- Inhibiting Hv1 channel in peripheral sensory neurons attenuates chronic inflammatory pain and opioid side effects.Cell research · 2022Article
- NOX1/NADPH Oxidase Promotes Synaptic Facilitation Induced by Repeated DThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Quercetin Ameliorates CFA-Induced Chronic Inflammatory Hyperalgesia via Modulation of ROS-Mediated ERK1/2 Signaling and Inhibition of Spinal Glial Activation In Vivo.Neuromolecular medicine · 2020Article
- 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
- Interplay between the Endogenous Opioid System and Proteasome Complex: Beyond Signaling.International journal of molecular sciences · 2019Review
- Antidotal effects of thymoquinone against neurotoxic agents.Interdisciplinary toxicology · 2018Review
- Reactive Oxygen Species as Intracellular Signaling Molecules in the Cardiovascular System.Current cardiology reviews · 2018Review
- Peroxiredoxin 6 mediates Gαi protein-coupled receptor inactivation by cJun kinase.Nature communications · 2017Article
- Therapeutic potential of NADPH oxidase 1/4 inhibitors.British journal of pharmacology · 2017Review
- Depressive-Like Behaviors Are Regulated by NOX1/NADPH Oxidase by Redox Modification of NMDA Receptor 1.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- Nitroxidative Signaling Mechanisms in Pathological Pain.Trends in neurosciences · 2016Review
- Regulation of morphine-induced synaptic alterations: Role of oxidative stress, ER stress, and autophagy.The Journal of cell biology · 2016Article
- Blockade of Serotonin 5-HTFrontiers in pharmacology · 2016Article
- Inhibition of the regulator of G protein signalling RGS4 in the spinal cord decreases neuropathic hyperalgesia and restores cannabinoid CB1 receptor signalling.British journal of pharmacology · 2015Article
- The σ1 receptor engages the redox-regulated HINT1 protein to bring opioid analgesia under NMDA receptor negative control.Antioxidants & redox signaling · 2015Article
- New insights on NOX enzymes in the central nervous system.Antioxidants & redox signaling · 2014Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The involvement of reactive oxygen species (ROS) in morphine-induced analgesia and tolerance has been suggested, yet how and where ROS take part in these processes remains largely unknown. Here, we report a novel role for the superoxide-generating enzyme NOX1/NADPH oxidase in the regulation of analgesia and acute analgesic tolerance. In mice lacking Nox1 (Nox1(-/Y)), the magnitude of the analgesia induced by morphine was significantly augmented. More importantly, analgesic tolerance induced by repeated administration of morphine was significantly suppressed compared with that in the littermates, wild-type Nox1(+/Y). In a membrane fraction obtained from the dorsal spinal cord, no difference was observed in morphine-induced [(35)S]GTPγS-binding between the genotypes, whereas morphine-stimulated GTPase activity was significantly attenuated in Nox1(-/Y). At 2 h after morphine administration, a significant decline in [(35)S]GTPγS-binding was observed in Nox1(+/Y) but not in Nox1(-/Y). No difference in the maximal binding and affinity of [(3)H]DAMGO was observed between the genotypes, but the translocation of protein kinase C isoforms to the membrane fraction following morphine administration was almost completely abolished in Nox1(-/Y). Finally, the phosphorylation of RGS9-2 and formation of a complex by Gαi2/RGS9-2 with 14-3-3 found in morphine-treated Nox1(+/Y) were significantly suppressed in Nox1(-/Y). Together, these results suggest that NOX1/NADPH oxidase attenuates the pharmacological effects of opioids by regulating GTPase activity and the phosphorylation of RGS9-2 by protein kinase C. NOX1/NADPH oxidase may thus be a novel target for the development of adjuvant therapy to retain the beneficial effects of morphine.
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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.