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• W2923333372 abstract "The management of chronic pain with opioids can cause opioid-induced analgesic tolerance (OIT) and hyperalgesia (OIH), which complicates clinical pain-management treatments. Although G-protein coupled receptors have been studied for years, the intracellular signaling pathways triggered by the activation of µ-opioid receptors are not well known. We sought to determine whether OIT is linked to a decreased activity in the PI3K/AKT intracellular signaling pathway. To assess this pathway, 25 C57BL/6 WT male mice (21 ± 4g) were divided into control (n=10, 1 μL saline) and experimental (n=10, 15 mg/kg of morphine; n=5, spinal nerve ligation (SNL) at the L4 vertebrae with 15 mg/kg of morphine) groups. Injections were given subcutaneously twice a day for a total of five days. Thermal paw withdrawal latency for each group was measured before and 0, 30, and 60 minutes post injection. Mice given morphine developed OIH and OIT after 3 days. The brainstem, spinal cord, dorsal root ganglia, and sciatic nerves were removed and processed for qPCR using primers for AKT1, AKT2, AKT3, PIK3cg v1, PIK3cg v2, PIK3cg v3, PTEN, and nNOS1. Significant increases and decreases in gene expression levels (p≤0.05) were seen in the brainstem of morphine tolerant mice without SNL. There was a decreased expression for AKT1 (p<0.05), AKT2 (p<0.05), PIK3cg v3 (p<0.01), PTEN (p<0.01), and nNOS1(p<0.05), and an increased expression of AKT3 (p<0.05) in the brainstem of morphine-tolerant mice without SNL. Current and future studies will be performed to evaluate the expression levels of cGMP, a downstream target of the PI3K/AKT pathway, in the spinal cord and DRG. Supported by grants from the National Institutes of Health (K01 DA 042902) and the University of Minnesota Undergraduate Research Opportunity Program. The management of chronic pain with opioids can cause opioid-induced analgesic tolerance (OIT) and hyperalgesia (OIH), which complicates clinical pain-management treatments. Although G-protein coupled receptors have been studied for years, the intracellular signaling pathways triggered by the activation of µ-opioid receptors are not well known. We sought to determine whether OIT is linked to a decreased activity in the PI3K/AKT intracellular signaling pathway. To assess this pathway, 25 C57BL/6 WT male mice (21 ± 4g) were divided into control (n=10, 1 μL saline) and experimental (n=10, 15 mg/kg of morphine; n=5, spinal nerve ligation (SNL) at the L4 vertebrae with 15 mg/kg of morphine) groups. Injections were given subcutaneously twice a day for a total of five days. Thermal paw withdrawal latency for each group was measured before and 0, 30, and 60 minutes post injection. Mice given morphine developed OIH and OIT after 3 days. The brainstem, spinal cord, dorsal root ganglia, and sciatic nerves were removed and processed for qPCR using primers for AKT1, AKT2, AKT3, PIK3cg v1, PIK3cg v2, PIK3cg v3, PTEN, and nNOS1. Significant increases and decreases in gene expression levels (p≤0.05) were seen in the brainstem of morphine tolerant mice without SNL. There was a decreased expression for AKT1 (p<0.05), AKT2 (p<0.05), PIK3cg v3 (p<0.01), PTEN (p<0.01), and nNOS1(p<0.05), and an increased expression of AKT3 (p<0.05) in the brainstem of morphine-tolerant mice without SNL. Current and future studies will be performed to evaluate the expression levels of cGMP, a downstream target of the PI3K/AKT pathway, in the spinal cord and DRG. Supported by grants from the National Institutes of Health (K01 DA 042902) and the University of Minnesota Undergraduate Research Opportunity Program." @default.
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• W2923333372 date "2019-04-01" @default.
• W2923333372 modified "2023-09-28" @default.
• W2923333372 title "(220) Involvement of the PI3K/AKT Signaling Pathway in the Peripheral and Central Nervous System in the Development of Morphine Tolerance" @default.
• W2923333372 doi "https://doi.org/10.1016/j.jpain.2019.01.141" @default.
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