Oxytocin, sold as Pitocin and Syntocinon, is a natural mammalian peptide hormone that acts primarily as a neurotransmitter in the brain. In 1953, oxytocin was the first polypeptide hormone synthesized in a lab. Oxytocin serves secondary physiological roles outside of the brain such as in uterine contractions, in genital tissue during sexual arousal, and as a mild antagonist to vasopressin. Oxytocin is used pharmaceutically to stimulate uterine contraction for labor induction or augmentation. In experimental settings oxytocin is being explored as a therapeutic tool for social issues in drug addiction and autism, and also to characterize the role of the oxytocin system in pleasure- and drug-seeking behaviors. Administering oxytocin in a controlled study allows a better understanding of social and reproductive behavior, stress response, and pair bonding. Oxytocin is administered via IV or IP injection in animals, and often given to humans as an intranasal spray.
In autism oxytocin has been demonstrated to improve scores on tests of emotional intelligence, and reinforce pro-social group behavior including group cooperation. Researchers are not sure whether many of these effects are specific to autism or a more general mechanism that might show an effect in other populations; effects like anxiety reduction, reduced hypothalamic-pituitary-adrenal axis responsiveness, reduced amygdala reactivity to social stimuli, and increased dopaminergic motivation to affiliate socially are plausible mechanisms that require more study in different populations.
Gaulthier et al found in subjects diagnosed with autism that specific areas of improvement included “decreased repetitive behaviours [and] enhanced emotional understanding of speech intonation”.
Oxytocin’s ability to enhance pro-social behavior may provide therapeutic benefits in other states of disorder or impairment:
OT based therapies of any class may be most beneficial for the treatment of social impairments as a pharmacological adjunct to behavioral therapies. It is hypothesized that OT acts to enhance the saliency of social information and to assign social stimuli a positive valence. In that capacity, many of the initial studies of OT on functional human social cognition have demonstrated short-term prosocial effects evident in discrete experimental measures, including socially reinforced learning
Modi and Young (2012) advise that oxytocin be considered and examined as a part of a larger strategy and integrated with other therapeutic modalities:
We propose that the saliency and valence effects of OT could enhance the acquisition of social skills taught as a part of structured behavior therapy program, like applied behavioral analysis. Many of the sub-skills already taught as a part of social skills training paradigms, like maintaining eye contact and understanding facial expressions, are modulated by OT
One proposed mechanism of oxytocin to enhance pro-social behavior is its involvement in dopaminergic reward, leading researchers to speculate that it may improve the reward effect experienced while being social. Administering oxytocin seems to reduce or modulate drug craving; it is possible a similar mechanism is at work:
utility of OXT in reducing consumption of and craving for a wide range of substances may lie in its ability to modulate drug-induced neurochemical effects within the mesolimbic dopamine pathway. 
Oxytocin is attractive to some researchers interested in better treatments for drug addictions, not only because of potential anti-addictive qualities, but also because recovering drug abusers may benefit from pro-social qualities, especially in their close relationships. Abuse of some drugs can lower and alter oxytocin, dopamine, and receptor expression and function:
We demonstrate that repeated exposure to the commonly abused psychostimulant amphetamine (AMPH) inhibits the formation of partner preferences (an index of pair bonding) .... [and] altered OT and DA neurotransmission in regions that mediate partner preference formation: it decreased OT and DA D2 receptor immunoreactivity in the medial prefrontal cortex (mPFC) and nucleus accumbens (NAcc), respectively, and increased NAcc DA levels. 
In this experimental model, the researchers found that administering oxytocin restored normal function of those physiological markers, including some functional markers of the dopamine system, as well as the formation of partner preferences.
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Feng C, Lori A, Waldman ID, Binder EB, Haroon E, Rilling JK. “A common oxytocin receptor gene (OXTR) polymorphism modulates intranasal oxytocin effects on the neural response to social cooperation in humans.” Genes Brain Behav. 2015 Sep;14(7):516-25.
Gauthier C, Doyen C, Amado I, Lôo H, Gaillard R.[Therapeutic effects of oxytocin in autism: Current status of the research]. [Article in French] Encephale. 2016 Jan 18. pii: S0013-7006(15)00128-1.
Modi ME, Young LJ. “The oxytocin system in drug discovery for autism: Animal models and novel therapeutic strategies” Horm Behav. 2012 Mar; 61(3): 340–350.
Peters ST, Bowen MT, Bohrer K, McGregor IS, Neumann ID. “Oxytocin inhibits ethanol consumption and ethanol-induced dopamine release in the nucleus accumbens.” Addict Biol. 2016 Jan 25.
Young KA, Liu Y, Gobrogge KL, Wang H, Wang Z. “Oxytocin reverses amphetamine-induced deficits in social bonding: evidence for an interaction with nucleus accumbens dopamine.” J Neurosci. 2014 Jun 18;34(25):8499-506.