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- W3176307716 abstract "Oxycodone is a prescription opioid that is widely used because of its substantial analgesic efficacy. However, it is accompanied by numerous side effects such as nausea, constipation, mioisis and respiratory depression, which can decrease patient compliance with treatment, affect quality of life and potentially lead to coma or death. These adverse effects are mediated by neurons in brain stem nuclei. Understanding changes in gene expression and signaling following chronic exposure will be helpful in developing therapeutic strategies to mitigate these effects. We have analyzed the effect of chronic oxycodone exposure on MAPK and mTOR as well as translational pathways in rat brain stem. We observed increase in phosphorylation of p38 and mTOR but not ERK1/2 kinases by oxycodone. Since p38 kinase is activated in response to cytokines or stress, our results suggest that oxycodone exposure triggers the cellular response to chronic stress. Analysis of translational regulation in rat brain stem revealed both stimulatory and inhibitory effects of chronic oxycodone exposure on various steps of translation. The possible mechanism of translational regulation of specific mRNAs by chronic oxycodone exposure in rat brain stem will be discussed. Supported by Department of Emergency Medicine and Department of Pharmacology, Toxicology and Neuroscience, Louisiana State University Health Sciences Center; Shreveport." @default.
- W3176307716 created "2021-07-05" @default.
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- W3176307716 date "2011-04-01" @default.
- W3176307716 modified "2023-09-26" @default.
- W3176307716 title "Chronic oxycodone exposure alters translational and signaling pathways in the rat brain stem" @default.
- W3176307716 doi "https://doi.org/10.1096/fasebj.25.1_supplement.lb414" @default.
- W3176307716 hasPublicationYear "2011" @default.
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