Sufficiently intense, frequent, or chronic consumption of alcohol or opioids induces a drug-dependent state in both humans and rodents, characterized by tolerance to drug effects and withdrawal symptoms upon cessation of use. The withdrawal syndrome associated with both alcohol and opioid dependence includes heightened pain sensitivity (i.e., hyperalgesia), which has been hypothesized to contribute to the motivation to seek and consume more drug through negative reinforcement processes (i.e., taking drug for relief). Clinical literature suggests a bidirectional relationship between chronic drug consumption and chronic pain sensitivity (see Koob, 2021, for review). While hyperalgesia in opioid dependence has been more extensively studied, recent work has begun to elucidate the neurobiology of alcohol-dependence–induced hyperalgesia (e.g., Avegno, 2018). We previously demonstrated that oxytocin administration could reduce alcohol consumption in alcohol-dependent rats (Tunstall et al., 2019). Based on oxytocin’s known analgesic effects within the central nervous system (Petersson, 1996; Poisbeau, 2018; Boll, 2018), we hypothesized that oxytocin could ameliorate alcohol-dependence–induced hyperalgesia. To test this hypothesis, we assessed the effects of central and peripheral oxytocin administration on thermal (Hargreaves assay) and mechanical (von Frey assay) pain sensitivity in rats rendered alcohol dependent through repeated cycles of alcohol vapor exposure. In parallel, we are testing manipulations of the brain’s oxytocin system for their effects on alcohol-motivated behavior and, separately, developing rodent models of opioid dependence to probe the role of neuropeptides in opioid dependence.

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