Rebalancing the Addicted Brain: Oxytocin Interference with the Neural Substrates of Addiction

Bowen, Michael T.; Neumann, Inga D.

doi:10.1016/j.tins.2017.10.003

Cited by 72 publications

(72 citation statements)

References 120 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In our previous sections we have presented strong preclinical evidence from our laboratories and others to suggest that exogenous administration of oxytocin reduces drug seeking and self-administration, tolerance, and reinstatement. Importantly, these effects occur across multiple drug classes and impact multiple neurotransmitter systems (dopamine, GABA, serotonin) indicating that oxytocin may be rebalancing an addicted brain through multiple dependent and interdependent mechanisms (Bowen & Neumann, 2017). Additionally, burgeoning research has exemplified the impact of oxytocin on social reward alone (Dolen et al, 2013; Hung et al, 2017).…”

Section: Discussionmentioning

confidence: 99%

“…Social factors can also have a profound impact on maintaining abstinence from drug use for some people. It is suggested that parallel brain circuits mediate social vs. drug reward-related behaviors and that oxytocin may act to redirect behaviors between these reward circuits (McGregor & Bowen, 2012), shift the preference for novel situations and experiences to one for familiarity (Tops et al, 2014), and rebalances the addicted brain (Bowen & Neumann, 2017). …”

Section: Oxytocin As a Treatment For Addictionmentioning

confidence: 99%

“…The central and peripheral oxytocin systems have been recently reviewed (Bowen & Neumann, 2017; Buisman-Pijlman et al, 2014; Knobloch & Grinevich, 2014), so we will only briefly describe the central system here. The neuropeptide oxytocin, produced by the precursor protein oxytocin/neurophysin I prepropeptide, consists of 9 amino acids.…”

Section: Introductionmentioning

confidence: 99%

“…Recent evidence suggests that it does to a limited extent and mechanisms underlying such penetration into brain are just recently coming into focus (Veening & Olivier, 2013). Central oxytocin synthesized in the SON is secreted into the bloodstream through neurohemal contact in response to reproductive behaviors, social stimuli, and stress (Bowen & Neumann, 2017). However, only 1–2% of oxytocin synthesized and released by peripheral organs (uterine epithelium, ovary, testis, vascular endothelium cells and heart) (Nishimori et al, 2008) and or by the posterior pituitary cross the blood–brain barrier (Ermisch et al, 1985; Landgraf, Ermisch, & Hess, 1979).…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Oxytocin and Rodent Models of Addiction

Leong

Cox

King

et al. 2018

International Review of Neurobiology

View full text Add to dashboard Cite

Interest for the use of oxytocin as a treatment for addiction began over 40years ago. Better known for its roles in parturition, lactation and pair bonding, oxytocin also has anxiolytic properties, reduces immune and inflammatory responses, and has a role in learning and memory. In this chapter, oxytocin effects on addiction processes are described by highlighting research findings that have used oxytocin within current preclinical animal models of addiction, relapse, or craving. First, we provide a brief background of the endogenous oxytocin system followed by descriptions of the behavioral models used to study addiction, including models of drug taking and seeking. Then we review recent preclinical studies that have used oxytocin as a therapeutic intervention throughout multiple stages of the addiction cycle from a behavioral and neurobiological perspective. These models encompass the entire range of the addiction cycle including acquisition and maintenance of drug taking, withdrawal and craving during periods of drug abstinence, and ultimately relapse. We then posit several theories about how oxytocin interacts with both drug and social reward, as well as presenting a mechanistic account of how specific oxytocin receptor localization may contribute to oxytocin's efficacy as an addiction therapeutic.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Oxytocin As a Treatment For Addictionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Oxytocin and Rodent Models of Addiction

Leong

Cox

King

et al. 2018

International Review of Neurobiology

View full text Add to dashboard Cite

show abstract

“…[191][192][193][194][195] Oxytocin administration into the ventral tegmental area 192 and in the nucleus accumbens core 196 has been shown to decrease deprivation-induced food intake and palatable sucrose intake in rats. 198 It has been shown that i.c.v. 198 It has been shown that i.c.v.…”

Section: Nucleus Accumbens and Ventral Tegmental Areamentioning

confidence: 99%

Role of oxytocin in the control of stress and food intake

Onaka

Takayanagi

2019

J Neuroendocrinology

View full text Add to dashboard Cite

Oxytocin neurones in the hypothalamus are activated by stressful stimuli and food intake. The oxytocin receptor is located in various brain regions, including the sensory information‐processing cerebral cortex; the cognitive information‐processing prefrontal cortex; reward‐related regions such as the ventral tegmental areas, nucleus accumbens and raphe nucleus; stress‐related areas such as the amygdala, hippocampus, ventrolateral part of the ventromedial hypothalamus and ventrolateral periaqueductal gray; homeostasis‐controlling hypothalamus; and the dorsal motor complex controlling intestinal functions. Oxytocin affects behavioural and neuroendocrine stress responses and terminates food intake by acting on the metabolic or nutritional homeostasis system, modulating emotional processing, reducing reward values of food intake, and facilitating sensory and cognitive processing via multiple brain regions. Oxytocin also plays a role in interactive actions between stress and food intake and contributes to adaptive active coping behaviours.

show abstract