Different roles of μ-, δ- and κ-opioid receptors in ethanol-associated place preference in rats exposed to conditioned fear stress

Effect of Selective Blockade of μ1 or δ Opioid Receptors on Reinstatement of Alcohol-Seeking Behavior by Drug-Associated Stimuli in Rats,

“…It has also consistently been shown that treatments with the selective 1 / 2 receptor antagonists ␤-funaltrexamine and CTOP, the 1 antagonist naloxonazine, or the selective ␦ receptor antagonists naltriben and naltrindole reduce ethanol consumption in rodents (Froehlich et al 1991;Hyytia 1993;KrishnamSarin et al 1995aKrishnamSarin et al , 1995bKrishnamSarin et al , 1998Honkanen et al 1996). In addition, a recent place conditioning study demonstrated that blockade of or ␦ receptors by ␤-funaltrexamine or naltrindole significantly attenuates ethanolinduced conditioned place preference (Matsuzawa et al 1999). Thus, several lines of evidence implicate both 1 and ␦ opioid receptors in the mediation of the rewarding effect of ethanol.…”

“…Selective or ␦ opioid receptor antagonists block ethanol-induced conditioned place preference and suppress the self-administration of ethanol in rats (Cunningham andPrather 1992, Hyytiä 1993;Krishnan-Sarin et al 1995a;1995b;Honkanen et al 1996;Krishnan-Sarin et al 1998;Matsuzawa et al 1998). Selective antagonists, on the other hand, exert an opposite effect and facilitate the expression of conditioned ethanol place preference (Matsuzawa et al 1999). Thus, existing evidence suggests that stimulation of and/or ␦ opioid receptors is linked to the positive reinforcing effects of ethanol, whereas activation of the opioid receptor family mediates aversive and dysphoric aspects of ethanol's actions.…”

The Role of Delta Opioid Receptors in Ethanol Consumption and Seeking: Implications for New Treatments for Alcohol Use Disorders

“…Dopamine release in the striatum is stimulated by ethanol, DOP-R agonists and enkephalinase inhibitors (Dourmap et al, 1990;Petit et al, 1986;Spanagel et al, 1990) and ethanol-induced release of dopamine in the striatum is blocked by DOP-R antagonists (Acquas et al, 1993;Widdowson & Holman, 1992). DOP-R agonists increase and DOP-R antagonists decrease, respectively, ethanolinduced place preference in rats (Bie et al, 2009;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b) and DOP-R antagonists can make a nonaversive dose of alcohol aversive (Froehlich et al, 1998). A series of studies demonstrated that the DOP-R plays a role in conditioned place preference (CPP) to ethanol using a model of conditioned fear stress (Matsuzawa et al, 1998;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b).…”

“…DOP-R agonists increase and DOP-R antagonists decrease, respectively, ethanolinduced place preference in rats (Bie et al, 2009;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b) and DOP-R antagonists can make a nonaversive dose of alcohol aversive (Froehlich et al, 1998). A series of studies demonstrated that the DOP-R plays a role in conditioned place preference (CPP) to ethanol using a model of conditioned fear stress (Matsuzawa et al, 1998;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b). In this model, ethanol produced a significant CPP only in rats that were exposed to an environment previously paired with an electric foot shock (Matsuzawa et al, 1998;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b).…”

“…A series of studies demonstrated that the DOP-R plays a role in conditioned place preference (CPP) to ethanol using a model of conditioned fear stress (Matsuzawa et al, 1998;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b). In this model, ethanol produced a significant CPP only in rats that were exposed to an environment previously paired with an electric foot shock (Matsuzawa et al, 1998;Matsuzawa et al, 1999a;Matsuzawa et al, 1999b). Significant CPP to ethanol (300 mg/kg, intraperitoneal (i.p.)…”