[3H]DPDPE binding to δ opioid receptors in the rat mesocorticolimbic and nigrostriatal pathways is transiently increased by acute ethanol administration

Ethanol exposure differentially alters pro-enkephalin mRNA expression in regions of the mesocorticolimbic system

“…The in vivo administration of a high dose of ethanol decreases [ 3 H] [D-Ala 2 ,MePhe 4 ,Gly-ol 5 ]-enkephalin ([ 3 H]-DAMGO) binding to μ receptors in the VTA and the shell region of the NAcc (NAccSh) and increases ligand binding in the prefrontal cortex (PFC), with different kinetics (Méndez et al 2001). In contrast, the same treatment increases [ 3 H] [2-D-penicillamine, 5-D-penicillamine]-enkephalin ([ 3 H]-DPDPE) binding to δ receptors in these regions 2 h after drug administration (Méndez et al 2004). These findings suggest that ethanol may differentially alter enkephalinergic and β-endorphinergic transmission and that these ethanolinduced changes may be region-specific.…”

“…Coronal brain sections (20 μ) were obtained in a cryostat and maintained at −70°C until assayed by in situ hybridization. All brain sections were obtained from animals used in previous studies (Méndez et al 2001(Méndez et al , 2004 as part of a large research project on the effects of ethanol on opioid peptide systems.…”

“…Animal treatment was performed as previously reported (Méndez et al 2001(Méndez et al , 2004. Briefly, adult male Wistar rats (250-300 g), fed ad libitum (Purina Chow) and maintained in a 12 h light-dark cycle, received a single acute dose of ethanol (2.5 g/kg body weight) (experimental group) or distilled water (control group) by oral administration with an intragastric cannula.…”

δ-Opioid Receptor Function in the Dorsal Striatum Plays a Role in High Levels of Ethanol Consumption in Rats

“…However, DOP-R agonists reportedly have higher analgesic activity in states of disrupted physiological conditions (Kamei et al, 1994. Stressors, morphine, and ethanol administration change the distribution of DOP-R from the cytoplasmic compartment to the plasma membrane and increase DOP-R activity (Commons, 2003;Méndez et al, 2004Méndez et al, , 2008Hack et al, 2005;Méndez and Morales-Mulia, 2006). As it is difficult to directly demonstrate the redistribution of DOP-R using immunohistochemistry due to nonspecific activity of DOP-R antibodies (Scherrer et al, 2009), we measured the ex vivo activity of the DOP-R using […”

“…A large body of evidence suggests the MOP-R plays a role in ethanol-mediated behaviors (Reid and Hunter, 1984;Gardell et al, 1996;Stromberg et al, 1998;Lê et al, 1999;Roberts et al, 2000;Hall et al, 2001;Becker et al, 2002;Ciccocioppo et al, 2002). Similarly, the DOP-R is dynamically regulated by ethanol exposure (Charness et al, 1993;Winkler et al, 1998;Méndez et al, 2004), is implicated in ethanol reward (Froehlich et al, 1991;Borg and Taylor, 1997;Froehlich et al, 1998;Matsuzawa et al, 1999a,b;Shippenberg et al, 2008), and plays a role in ethanol self-administration. DOP-R antagonists have been shown to have mixed effects on ethanol consumption and seeking in rats; some studies have shown they reduce ethanol consumption and seeking (Krishnan-Sarin et al, 1995a,b;Franck et al, 1998;June et al, 1999;Hyytiä and Kiianmaa, 2001;Ciccocioppo et al, 2002;Nielsen et al, 2012), while other studies have not shown this effect (Stromberg et al, 1998;Ingman et al, 2003;Margolis et al, 2008).…”