Chronic pain and excessive alcohol consumption are individually problems in our society today. Alcohol Use Disorder (AUD) affects 15.1 million adult Americans each year. Chronic pain affects over 100 million people annually in the United States. However, there is growing evidence suggesting that these two conditions can often be interrelated with chronic pain increasing consumption of alcohol, and excessive alcohol consumption increasing pain that leaves a feedback cycle trapping millions of patients in an ever worsening spiral. Large population-based studies show an association between pain and alcohol abuse, suggesting a link between increased alcohol use and reduced pain. While rodent studies consistently demonstrate antinociception following acute ethanol administration in hot-plate and tail-flick tests. However, little is currently known about the effects of alcohol in chronic pain models. We hypothesize that acute ethanol administration will possess analgesic-like properties in models of chronic pain by engaging opioid receptors in addition to its more commonly studied action at the GABA receptor. The first aim of this study was to characterize the antinociceptive effects of alcohol in Complete Freund’s Adjuvant (CFA) and Chronic Constriction Injury (CCI) mouse models of chronic inflammatory and neuropathic pain models, respectively. The second aim of this study is to investigate the mechanisms behind ethanol's analgesic like effects including tolerance, receptor activation and correlates with blood alcohol content. Lastly, we investigated whether alcohol maintains its analgesic-like effects in non-reflexive assays in addition to effects in reflexive assays.