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- W2551668281 endingPage "879" @default.
- W2551668281 startingPage "862" @default.
- W2551668281 abstract "Tissue injury can initiate bidirectional signaling between neurons, glia, and immune cells that creates and amplifies pain. While the ability for neurotransmitters, neuropeptides, and cytokines to initiate and maintain pain has been extensively studied, recent work has identified a key role for reactive oxygen and nitrogen species (ROS/RNS; nitroxidative species), including superoxide, peroxynitrite, and hydrogen peroxide. In this review we describe how nitroxidative species are generated after tissue injury and the mechanisms by which they enhance neuroexcitability in pain pathways. Finally, we discuss potential therapeutic strategies for normalizing nitroxidative signaling, which may also enhance opioid analgesia, to help to alleviate the enormous burden of pathological pain." @default.
- W2551668281 created "2016-11-30" @default.
- W2551668281 creator A5009768215 @default.
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- W2551668281 creator A5051353828 @default.
- W2551668281 creator A5062898531 @default.
- W2551668281 creator A5091505369 @default.
- W2551668281 date "2016-12-01" @default.
- W2551668281 modified "2023-10-14" @default.
- W2551668281 title "Nitroxidative Signaling Mechanisms in Pathological Pain" @default.
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