A new study in the journal Biological Psychiatry suggests that inhibiting the hormone oxytocin may help people to recover from unpleasant, stressful, or traumatic social situations.
Oxytocin is known as the “love hormone.” The chemical – which also acts as a neurotransmitter – received its popular name because we secrete it when we cuddle with our loved ones or stare into their eyes.
Oxytocin has also been shown to have other, prosocial benefits. For example, in people with autism, it was found to promote social behavior, and a study that Medical News Today reported on found that oxytocin may increase our empathy.
But oxytocin does not always encourage social bonding. Studies have shown that, when exposed to stressful social situations, female mice exhibit increased activity in oxytocin-producing neurons and tend to avoid subsequent unfamiliar social situations.
These findings corresponded with what happened when female mice received oxytocin intranasally: they displayed reduced social interaction after a stressful social event.
New research – jointly led by Natalia Duque-Wilckens and Brian Trainor, who are both behavioral neuroscientists at the University of California, Davis – goes further and suggests that blocking the neurotransmitter may, in fact, help people to recover from social anxiety.
The researchers’ hypothesis is that oxytocin, rather than simply promoting social bonds, amplifies the effects of both positive and negative social interactions.
This, according to the team, explains why the neurotransmitter is known as the love hormone but can also promote social aloofness after a negative, stressful social experience.
The new study also aimed to uncover the neurobiological basis for such a theory. As expected, the researchers found that two different brain areas are affected differently by oxytocin.
Previous studies, as referenced by the authors, have shown that heightened oxytocin activity in a brain area called the nucleus accumbens promotes the rewarding aspects of positive social interactions.
The new research further confirmed these studies. Duque-Wilckens and her colleagues inhibited oxytocin by administering an oxytocin receptor antagonist to male and female California mice.
These mice had been exposed to so-called social defeat, which is a procedure wherein a smaller rodent is placed in the cage of a larger, more aggressive, territorial rodent.
The team used immunohistochemistry to examine when and where oxytocin was activated. In the females, the researchers found two brain regions in which oxytocin was more active: the nucleus accumbens, and the bed nucleus of the stria terminalis (BNST).
Interestingly, when the researchers injected the oxytocin inhibitor into the BNST but not in the nucleus accumbens, female mice were more likely to interact with new mice after the stressful event.
Blocking oxytocin, therefore, “increased social approach and decreased social vigilance responses,” write the authors.
Trainor says that these results are very encouraging, because “for antidepressants like Prozac to have this same effect, it takes a month of daily treatment.”
As the authors conclude, “Our results suggest that [oxytocin receptor] activation in anteromedial BNST induces a vigilance response in which individuals avoid, yet attend to unfamiliar social contexts.”
“Our results suggest that [oxytocin receptor] antagonists may have unappreciated therapeutic potential for stress-induced psychiatric disorders,” they add.
“Stressful social experiences appear to change which parts of the brain use oxytocin […] Understanding how this works in a mouse gives us new ideas on how we could use drugs targeting oxytocin to reduce social anxiety.”