Differential expression of μ-opioid receptors in the nucleus accumbens, amygdala and VTA depends on liking for alcohol, chronic alcohol intake and estradiol treatment.

Affectations of the opioid system have been related to exacerbated alcohol consumption. The objectives of this work were to assess whether a deficit of β-endorphinergic neurons differentially affects alcohol intake in female rats with low (LC) and high alcohol consumption (HC), and to determine changes in the μ-opioid receptors (MOR) related to alcohol consumption and chronic exposure to alcohol in structures of the mesolimbic system. Female wild-type rats were selected according to their baseline alcohol intake levels and then exposed to chronic voluntary alcohol consumption after a single injection of either the vehicle or estradiol valerate (EV) to produce a β-endorphin neuronal deficit. Changes in alcohol consumption and MOR expression levels were assessed in the nucleus accumbens (NAc), amygdala (Amy) and ventral tegmental area (VTA) at 5 and 10 weeks after EV treatment. The LC rats increased alcohol intake from baseline to the initial weeks after EV treatment and this consumption remained stable throughout the studied period. In contrast, alcohol consumption increased steadily over time in the HC rats. The HC vehicle rats had a 38% higher MOR protein expression in the NAc than the LC vehicle rats. In addition, chronic alcohol consumption increased MOR expression in the Amy regardless of consumption level, whereas EV treatment produced a decrease in MOR expression in the VTA in all groups. These results suggest intrinsic differences in MOR expression related to alcohol consumption levels. Also, the EV treatment and chronic exposure to alcohol produced adaptive changes in MOR expression.