Abstract
Purpose
Alcohol use disorders (AUDs) are influenced by factors that can initiate, maintain, or induce relapse. Chronic pain has been linked to AUD as both a risk factor and a consequence of prolonged alcohol exposure. Pain share common neurological pathways with AUDs, and, in fact, alters the functioning of the mesolimbic dopaminergic system suggesting a plausible interaction. This study aims to investigate the effect of inflammatory pain on long-term alcohol intake in rats without prior alcohol consumption and observe changes in mesolimbic dopaminergic transmission.
Methods
Inflammatory pain was induced in eight-week-old Sprague Dawley rats using complete Freund adjuvant (CFA), while controls received saline. Two protocols were followed: one group had continuous access to 20% ethanol for one month (n = 10 per sex), and the second group for three months (n = 8 per sex) in a two-bottle choice paradigm. Mechanical nociception was assessed weekly using the Von Frey test. Dopamine levels in the nucleus accumbens core were measured through microdialysis during the final 1.5 months of ethanol exposure in the second cohort.
Results
After a month of alcohol exposure, rats showed no differences in alcohol consumption. However, from the second month until the end, rats exhibited a non-sex-dependent decrease in alcohol intake, significantly lower in CFA-animals. This reduction was accompanied by a blunted ethanol-evoked dopamine release in the nucleus accumbens.
Conclusion
These findings provide insights into the effect of pain on alcohol-elicited neurochemical responses and drinking behaviour, showing how pain alters dopamine response to alcohol, affecting drinking patterns and prolonging nociception from CFA.