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- W2024776507 abstract "Opioids have been used as potent analgesics in clinics for decades; however, their long-term administration leads to tolerance. Two possible mechanisms for drug tolerance are postulated as within-system and between-systems adaptation. The within-system tolerance is involved in the signal transduction of opioid receptors, including downregulation of opioid receptors, uncoupling of G-protein from opioid receptors, and β-arrestin recruitment to opioid receptors, which causes receptor desensitization and internalization/endocytosis. The between-systems tolerance comprehends the glutamatergic receptor system and glial activation with the release of proinflammatory cytokines, and thus the analgesic effect of morphine is reduced. Tumor necrosis factor-α (TNF-α) is a vital proinflammatory cytokine and exerts either a neurotoxic or neuroprotective effect on different diseases of the central nervous system. TNF-α has also been demonstrated to correlate with neuronal plasticity via activation of spinal glial cells and enhancement of glutamatergic transmission. Previous studies had revealed an increased expression of TNF-α in morphine tolerance. This review article focuses on the role of TNF-α in neuroinflammation and the glutamatergic receptor system in morphine tolerance. It may provide another adjuvant therapy for morphine tolerance, which extends the effectiveness of opioids in clinical pain management." @default.
- W2024776507 created "2016-06-24" @default.
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- W2024776507 creator A5053645631 @default.
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- W2024776507 date "2012-12-01" @default.
- W2024776507 modified "2023-10-01" @default.
- W2024776507 title "Role of neuroinflammation in morphine tolerance: Effect of tumor necrosis factor-α" @default.
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- W2024776507 doi "https://doi.org/10.1016/j.aat.2012.12.004" @default.
- W2024776507 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23385041" @default.
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