Priority communicationBuprenorphine Reduces Alcohol Drinking Through Activation of the Nociceptin/Orphanin FQ-NOP Receptor System
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Animals
Male, genetically selected, alcohol-preferring rats were used. They were bred at the Department of Pharmacological Sciences and Experimental Medicine of the University of Camerino (Marche, Italy) for 53 generations from Sardinian alcohol-preferring rats of the 13th generation, provided by the Department of Neurosciences of the University of Cagliari, Italy (Agabio et al 1996, Lobina et al 1997). These animals are referred to as Marchigian Sardinian alcohol-preferring (msP) rats. At the time of
Experiment 1: Effect of Acute IP Injections of Buprenorphine on Voluntary Alcohol Intake
The overall ANOVA revealed a highly significant treatment effect [F(4,9) = 22,31, p < .001]. Post-hoc analysis showed a significant dualistic effect with an increase of ethanol consumption after administration of .03 and .3 mg/kg of buprenorphine (p < .01) and a decrease of drinking after treatment with 3.0 and 6.0 mg/kg of the drug (p < .05). As shown in Figure 1, at the two lowest doses, buprenorphine significantly increased ethanol drinking throughout the 2-hour observation, whereas
Discussion
We report a dualistic action of buprenorphine on ethanol consumption. At low doses (.03 and .3 mg/kg), this drug increased ethanol consumption, whereas at the dose of 3.0 mg/kg, it markedly and selectively decreased it. Food and water consumption as well as motor behavior as assessed in the open field were not influenced in these animals after treatment with 3.0 mg/kg of buprenorphine. If the drug is given at higher doses (6.0 mg/kg), it further reduces ethanol consumption but food intake is
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2017, NeuropharmacologyCitation Excerpt :At low doses, it increased ethanol drinking in alcohol-preferring rats, an effect found with μ agonists and that was blocked by pretreatment with naltrexone. Conversely, at high doses, buprenorphine decreased ethanol intake, and this effect was not modified by naltrexone but was blocked by pretreatment with a selective NOP receptor antagonist, suggesting the NOP against properties of buprenorphine may offer a target for medication development (Ciccocioppo et al., 2007). Varenicline is a partial α4β2 nAChR agonist that decreases relapse rates in smoking cessation in humans (Jorenby et al., 2006).