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Association between the A 107 V substitution in the δ‐opioid receptors and ethanol drinking in mice selected for high and low analgesia
Author(s) -
Sacharczuk Mariusz,
Lesniak Anna,
Lipkowski Andrzej W.,
Korostynski Michal,
Przewlocki Ryszard,
Sadowski Bogdan
Publication year - 2014
Publication title -
addiction biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.445
H-Index - 78
eISSN - 1369-1600
pISSN - 1355-6215
DOI - 10.1111/adb.12030
Subject(s) - ethanol , endogenous opioid , receptor , opioid , opioid receptor , pharmacology , conditioned place preference , basal (medicine) , chemistry , medicine , alcohol , endocrinology , biochemistry , insulin
Experimental evidence suggests that endogenous opioids play an important role in the development of ethanol addiction. In this study, we employed two mouse lines divergently bred for opioid‐mediated stress‐induced analgesia. In comparison with HA (high analgesia line) mice, LA (low analgesia line) mice, having lower opioid receptor system activity, manifest enhanced basal as well as stress‐induced ethanol drinking. Here, we found that recently discovered C 320 T transition in exon 2 of the δ‐opioid receptor gene ( EU 446125.1), which results in an A 107 V substitution ( ACA 23171.1), leads to higher ethanol preference in CT mice compared with CC homozygotes. This genetic association is particularly evident under chronic mild stress ( CMS ) conditions. The interaction between stress and ethanol intake was significantly stronger in HA than in LA mice. Ethanol almost completely attenuated the pro‐depressive effect of CMS (assessed with the tail suspension test) in both the CC and CT genotypes in the HA line. In the LA mice, a lack of response to ethanol was observed in the CC genotype, whereas ethanol consumption strengthened depressive‐like behaviours in CT individuals. Our results suggest that constitutively active A 107 V substitution in δ‐opioid receptors may be involved in stress‐enhanced vulnerability to ethanol abuse and in the risk of ethanol dependence.