Abstract
Development of better treatments for alcohol use disorder (AUD) is urgently needed. One promising opportunity for this development is the potential of targeting the oxytocin peptide system. Preclinical studies showed that administration of exogenous oxytocin or, more recently, stimulation of neurons expressing endogenous oxytocin lead to a decreased alcohol consumption across several rodent models. Initial clinical studies also showed that administration of oxytocin decreased craving for alcohol and heavy alcohol drinking. However, several more recent clinical studies were not able to replicate these effects. Thus, although targeting the oxytocin system holds promise for the treatment of AUD, more nuanced approaches toward development and application of these treatments are needed. In this mini-review we discuss potential caveats resulting in differential success of attempts to use oxytocin for modulating alcohol use disorder-related behaviors in clinical studies and evaluate three directions in which targeting the oxytocin system could be improved: (1) increasing potency of exogenously administered oxytocin, (2) developing oxytocin receptor agonists, and (3) stimulating components of the endogenous oxytocin system. Both advances and potential pitfalls of these directions are discussed.
Highlights
Alcohol use disorder (AUD) is a devastating condition where the affected individuals continue to engage in drinking despite the negative experience and the harm caused by drinking
More than 5% of all deaths have been attributed to alcohol consumption [1]
Recent basic science studies revised our understanding of organization of the OXT system [29] and exogenous OXT’s penetrance into the brain [30, 31]. The goal of this minireview is to critically analyze the potential pitfalls associated with clinical studies testing effects of OXT on signs of AUD (Table 1) and to evaluate different directions of overcoming these pitfalls: by increasing potency of exogenously administered OXT, by developing OXT receptor (OXTR) agonists, and by stimulating the endogenous OXT system (Figure 1)
Summary
Alcohol use disorder (AUD) is a devastating condition where the affected individuals continue to engage in drinking despite the negative experience and the harm caused by drinking. Initial clinical studies indicated that OXT administration in humans could decrease signs of withdrawal and craving and inhibit excessive alcohol drinking [12, 17, 25]. The goal of this minireview is to critically analyze the potential pitfalls associated with clinical studies testing effects of OXT on signs of AUD (Table 1) and to evaluate different directions of overcoming these pitfalls: by increasing potency of exogenously administered OXT, by developing OXT receptor (OXTR) agonists, and by stimulating the endogenous OXT system (Figure 1).
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