Alcohol-use disorder : new treatment targets the oxytocin system

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Oxytocin research has experienced a remarkable resurgence over the past decade, particularly with respect to its role in regulating social cognition and its prospects for treating psychiatric disorders.

The oxytocin system has long been the focus of rigorous scientific investigation as a model of neurosecretion from the pituitary and for its role in regulating uterine contractions during labor and milk ejection during nursing.

Beginning in the mid-1960s, oxytocin became the focus of behavioral studies with an early emphasis on its influence on learning and memory (1).

By the late 1970s, pioneering studies in rats and sheep revealed that oxytocin not only leads to birth and successful nursing but also transforms the mother’s brain so that she is motivated to nurture the infant and develops selective mother-infant bonds (25); this area of research continues to evolve today (6).

Subsequent research in monogamous prairie voles revealed a central role in the formation of pair bonds between mates (7).

With the development of oxytocin mutant mice, the more subtle role of oxytocin in facilitating social recognition and social information processing became apparent (8).

The role of oxytocin in regulating social relationships has been extended to facilitate the bond between dogs and their owners (9).

More recent exquisite molecular and cellular studies have begun to reveal the precise mechanisms by which oxytocin modulates signal to noise in neural circuits to facilitate information processing (10).

tating social recognition and social information processing became apparent (8).

The role of oxytocin in regulating social relationships has been extended to facilitate the bond between dogs and their owners (9).

More recent exquisite molecular and cellular studies have begun to reveal the precise mechanisms by which oxytocin modulates signal to noise in neural circuits to facilitate information processing (10).

The neuropeptide oxytocin blocks enhanced drinking in alcohol-dependent rats, according to a study published April 16 in the open-access journal PLOS Biology led by Drs. Tunstall, Koob and Vendruscolo of the National Institutes of Health, and Drs. Kirson and Roberto of The Scripps Research Institute.

Targeting the oxytocin system, the authors note, may provide novel pharmaceutical interventions for the treatment of alcohol-use disorder.

Administering oxytocin can decrease consumption, withdrawal symptoms, and drug-seeking behavior associated with several drugs of abuse, and shows promise as a pharmacological approach to treat drug addiction.

But first, researchers need to understand how oxytocin mediates these effects in animal models.

To address this question, Tunstall and colleagues tested the hypothesis that oxytocin administration could normalize the maladaptive brain changes that occur in alcohol dependence and thereby reduce alcohol drinking in an established rat model of alcohol dependence.

The authors investigated oxytocin’s effects on dependence-induced alcohol consumption and altered signaling of the inhibitory neurotransmitter GABA in the central nucleus of the amygdala (CeA) – a key brain region in the network affected by alcohol dependence.

The experiments demonstrated that oxytocin administered systemically, intranasally or into the brain blocked excess drinking in alcohol-dependent but not in normal rats. Moreover, oxytocin blocked GABA signaling in the CeA.

Taken together, these results provide evidence that oxytocin likely blocks enhanced drinking by altering CeA GABA transmission.

These results provide evidence that aberrations in the oxytocin system may underlie alcohol use disorder and that targeting this system, possibly by intranasal administration, could prove a promising therapy in people who misuse alcohol.

More information: Tunstall BJ, Kirson D, Zallar LJ, McConnell SA, Vendruscolo JCM, Ho CP, et al. (2019) Oxytocin blocks enhanced motivation for alcohol in alcohol dependence and blocks alcohol effects on GABAergic transmission in the central amygdala. PLoS Biol 17(4): e2006421. doi.org/10.1371/journal.pbio.2006421
Journal information: PLoS Biology
Provided by Public Library of Science

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