Although the bidirectional relationship of alcohol and pain is clearly defined, the mechanisms behind this relationship remain poorly understood. Additionally, research regarding the relationship between alcohol and pain has largely focused on pain in the context of alcohol use disorder (AUD). Because both chronic pain patients and high-risk alcohol drinkers report drinking alcohol to alleviate their pain, understanding the mechanisms behind the pain relieving effects of alcohol is critical to improving pain management and preventing the progression of recreational alcohol drinking to AUD.

The Edwards Lab has previously shown a temporal shift in the analgesic properties of consumed alcohol over the course of persistent inflammatory pain. Unknown is whether the anti-nociceptive effects of alcohol modify pain avoidance behavior in the presence of persistent inflammatory pain and what the temporal neuroadaptations resulting from acute alcohol administration during early and late stages of persistent inflammatory pain are. These ongoing experiments, funded by an F31 award from the NIAAA, are investigating the basolateral amygdala as a neural locus mediating the anti-nociceptive effects of alcohol in the context of persistent inflammatory pain in female and male rats.

Specific Aim 1: To test the hypothesis that acute alcohol reduces chronic inflammatory pain via decreases in BLA activation.

Specific Aim 2: To test the hypothesis that acute alcohol and eCB signaling in the BLA reduce chronic inflammatory pain.