2006
DOI: 10.1016/j.pbb.2006.07.028
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Effect of acute administration of ethanol on beta-endorphin plasma level in ethanol preferring and non-preferring rats chronically treated with naltrexone

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Cited by 23 publications
(14 citation statements)
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“…Further, elevated frontal/temporal cortical μ-opioid receptor binding has been observed in cocaine dependence, the degree of which was shown to positively correlate with self-reported cocaine craving (Gorelick et al, 2005), and relate to relapse following treatment (Ghitza et al, 2010;Gorelick et al, 2008). NTX has been shown to block ethanol-induced β-endorphin and subsequent dopamine release in the nucleus accumbens and provide a blockade of ethanol-induced β-endorphin inhibition of GABAergic inhibitory interneurons in the ventral tegmental area (Johnson, 2008;Zalewska-Kaszubska et al, 2006). The decrease in amphetamine-induced dopamine Figure 3 Subjective response scores (drug effects questionnaire (DEQ)), presented with standard errors, at baseline (BA) and change from baseline at 5,10,15,20,30,60,90, and 120 min following methamphetamine (MA) administration, during both placebo and naltrexone (NTX) conditions.…”
Section: Discussionmentioning
confidence: 99%
“…Further, elevated frontal/temporal cortical μ-opioid receptor binding has been observed in cocaine dependence, the degree of which was shown to positively correlate with self-reported cocaine craving (Gorelick et al, 2005), and relate to relapse following treatment (Ghitza et al, 2010;Gorelick et al, 2008). NTX has been shown to block ethanol-induced β-endorphin and subsequent dopamine release in the nucleus accumbens and provide a blockade of ethanol-induced β-endorphin inhibition of GABAergic inhibitory interneurons in the ventral tegmental area (Johnson, 2008;Zalewska-Kaszubska et al, 2006). The decrease in amphetamine-induced dopamine Figure 3 Subjective response scores (drug effects questionnaire (DEQ)), presented with standard errors, at baseline (BA) and change from baseline at 5,10,15,20,30,60,90, and 120 min following methamphetamine (MA) administration, during both placebo and naltrexone (NTX) conditions.…”
Section: Discussionmentioning
confidence: 99%
“…Further, alcohol intake increases beta-endorphin release in brain regions such as the nucleus accumbens [22][23][24], an effect that is blocked by naltrexone [25]. Mu receptor antagonists such as naltrexone and naloxone also suppress ethanol intake across a wide range of animal paradigms [26][27][28][29][30][31][32][33][34][35][36] cf.…”
Section: Opioids: Mu Receptor Antagonist -Naltrexone Basic Science Anmentioning
confidence: 99%
“…Treatment of Warsaw High and Low Alcohol Preferring rats with the opioid antagonist naltrexone, stopped the plasma β-endorphin increase after EtOH administration in low-preference rats, and normalized β-endorphin plasma levels in high-preferring rats so that before and after alcohol exposure plasma levels were similar. These results indicate the clinical effectiveness of naltrexone in treatment of alcoholism may in part be due to both normalization of plasma β-endorphin levels and an attenuation of alcohol-rewarding properties (Zalewska-Kaszubska et al, 2006). In the same strains of rats, β-endorphin levels and EtOH intake were examined following treatment with acamprosate, which is approved for relapse prevention in withdrawing alcoholics.…”
Section: β-Endorphin and Acute Alcohol Exposurementioning
confidence: 90%
“…Opioids are primarily known for their analgesic properties, but they are highly implicated in the physiological rewarding effects of alcohol and other drugs of abuse (Wei & Loh, 1976;Van Ree, 1979;Zalewska-Kaszubska et al, 2006;see Crabbe et al, 2006 for review) as well as a wide array of other behavioral states. One class of endogenous opioids is the endorphins.…”
Section: The Hypothalamo-pituitary-adrenocortical Axis and -Endorphinmentioning
confidence: 99%