Binge-Like Exposure to Ethanol Enhances Morphine's Anti-nociception in B6 Mice.


:Elevation of the blood ethanol concentration (BEC) to > 80 mg/dL (17.4 mM) after binge drinking enhances inflammation in brain and neuroimmune signaling pathways. Morphine abuse is frequently linked to excessive drinking. Morphine exerts its actions mainly via the seven transmembrane G-protein-coupled mu opioid receptors (MORs). Opioid use disorders (OUDs) include combination of opioids with alcohol, leading to opioid overdose-related deaths. We hypothesized that binge drinking potentiates onset and progression of OUD. Using C57BL/6J (B6) mice, we first characterized time-dependent inflammatory gene expression change as molecular markers using qRT-PCR within 24 h after binge-like exposure to high-dose, high-concentration ethanol (EtOH). The mice were given one injection of EtOH (5 g/kg, 42% v/v, i.g.) and sacrificed at 2.5 h, 5 h, 7.5 h, or 24 h later. Inflammatory cytokines interleukin (IL)-1β, IL-6, and IL-18 were elevated in both the striatum (STr) and the nucleus accumbens (NAc) of the mice. We then investigated the expression profile of MOR in the STr at 2 min, 5 h, or 24 h after the first EtOH injection and at 24 h and 48 h after the third injection. This binge-like exposure to EtOH upregulated MOR expression in the STr and NAc, an effect that could enhance morphine's anti-nociception. Therefore, we examined the impact of binge-like exposure to EtOH on morphine's anti-nociception at the behavioral level. The mice were treated with or without 3-d binge-like exposure to EtOH, and the anti-nociceptive changes were evaluated using the hot-plate test 24 h after the final (3rd) EtOH injection with or without a cumulative subcutaneous dose (0, 0.1, 0.3, 1.0, and 3.0 mg/kg) of morphine at intervals of 30 min. The response curve of the mice given EtOH was shifted to the left, showing enhanced latency to response to morphine up to 3 mg/kg. Furthermore, co-treatment with the MOR antagonist naltrexone blocked morphine's anti-nociception in animals given either EtOH or saline. This confirms that MOR is involved in binge-like exposure to EtOH-induced changes in morphine's anti-nociception. Our results suggest that EtOH enhanced latency to analgesic response to morphine, and such effect might initiate the onset and progression of OUDs.


Front Psychiatry


Frontiers in psychiatry


Chang SL,Huang W,Han H,Sariyer IK




Has Abstract


2019-01-22 00:00:00








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    authors: Baetens I,Decruy C,Vatandoost S,Vanderhaegen B,Kiekens G

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    authors: Joshi YB,Light GA

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    authors: Görgen SM,Joormann J,Hiller W,Witthöft M

    更新日期:2015-07-07 00:00:00

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    authors: Hedderich DM,Drost R,Goldhardt O,Ortner M,Müller-Sarnowski F,Diehl-Schmid J,Zimmer C,Förstl H,Yakushev I,Jahn T,Grimmer T

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    authors: Sampogna G,Fiorillo A,Luciano M,Del Vecchio V,Steardo L Jr,Pocai B,Barone M,Amore M,Pacitti F,Dell'Osso L,Di Lorenzo G,Maj M,LIFESTYLE Working Group.

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    pub_type: 杂志文章


    authors: Smith S,Woodside DB

    更新日期:2021-01-08 00:00:00