Clinical studies have postulated that β-endorphin deficiency generates excessive alcohol consumption and, it has been shown that the reduction of β-endorphin neurons increases alcohol intake in animal models. The β-endorphin produce their rewarding effect when they act mainly on the μ-opioid receptors (MOR) located in mesolimbic structures. Thus, it is possible that individual differences in these components of the endogenous opioid system are related to different levels of alcohol consumption. The present study thus examines the relation between two levels of alcohol consumption and intrinsic characteristics of the components of the opioid system in outbred Wistar rats that were not genetically-selected. We analyzed the number of β-endorphin positive neurons in the arcuate nucleus (ArN) and the expression of mu opioid receptors (MOR) in regions of the reward system, such as the nucleus accumbens (NAc), amygdala (Amy), and ventral tegmental area (VTA) in outbred rats with low (LC) or high (HC) voluntary alcohol consumption. Findings showed that the HC rats had a lower number of β-endorphin positive neurons in the hypothalamic ArN and a higher expression of MOR in the NAc and VTA, compared to the LC rats. No changes in the expression of MOR in the Amy were observed between the two groups. Results suggest that intrinsic variability in the number of β-endorphin neurons and in the expression of MOR in the LC and HC rats, could explain their different patterns for alcohol intake.
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