Oxytocin Implicated in Rewarding Social Interaction
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people so sociable while others are loners or seemingly outright
allergic to interactions with others?
A new study in mice by researchers at the Stanford University School of Medicine
begins to provide an answer, pinpointing places and processes in the
brain that promote socialization by providing pleasurable sensations
when it occurs. The findings point to potential ways of helping people,
such as those with autism or schizophrenia, who can be painfully averse
to socializing.
The study, which was published Sept. 29 in Science, details the role of a substance called oxytocin in fostering and maintaining sociability. The senior author is Robert Malenka,
MD, PhD, professor and associate chair of psychiatry and behavioral
science. The lead author is former postdoctoral scholar Lin Hung, PhD.
“Our study reveals news about the brain circuitry behind social
reward, the positive experience you often get when you run into an old
friend or meet somebody you like,” said Malenka, who has focused much of
his research on an assembly of interacting nerve tracts in the brain
collectively known as the reward circuitry.
“The reward circuitry is crucial to our survival because it rewards
us for doing things that have, during our evolutionary history, tended
to enhance our survival, our reproduction and the survival of our
resulting offspring,” said Malenka, who holds the Nancy Friend Pritzker
Professorship in Psychiatry and the Behavioral Sciences. “It tells us
what’s good by making us feel good. When you’re hungry, food tastes
great. When you’re thirsty, water is refreshing. Sex is great pretty
much most of the time. Hanging out with your friends confers a survival
advantage, too, by decreasing your chances of getting eaten by
predators, increasing your chances of finding a mate and maybe helping
you learn where food and water are.”
Reward system conserved over evolution
Because the reward system is so critical, it’s been carefully
conserved over evolution and in many respects operates just the same way
in mice as it does in humans, making mice good experimental models for
studying it.
Far and away the most important component of the brain’s reward
circuitry, Malenka said, is a nerve tract that runs from a structure
deep in the brain called the ventral tegmental area to a midbrain
structure called the nucleus accumbens. The ventral tegmental area
houses a cluster of nerve cells, or neurons, whose projections to the
nucleus accumbens secrete a substance called dopamine, altering neuronal
activity in this region. Dopamine release in the nucleus accumbens can
produce a wave of pleasure, telling the brain that the event going on is
helpful for survival. Dopamine release in this region, and subsequent
changes in activity there and in downstream neurons, also primes the
brain to remember the events and the behaviors leading up to the
chemical’s release.
This tract, so famous for reinforcing survival-enhancing behaviors
such as eating, drinking and mating, has been infamously implicated in
our vulnerability to drug addiction — a survival-threatening outcome
resulting from drugs’ ability to inappropriately stimulate dopamine
secretion in the tract. But understanding exactly how and under what
natural conditions the firing of its dopamine-secreting nerves gets
tripped off is a work in progress.
Earlier work has specifically implicated dopamine release in the
nucleus accumbens in social behavior. “So, we knew reward circuitry
plays a role in social interactions,” Malenka said. “What we still
didn’t know — but now we do — was: How does this increased dopamine
release during social interaction come about?
‘Love hormone’ pulls the strings
Oxytocin is sometimes called the “love hormone” because it’s thought
to be involved in falling in love, mother-child bonding and sexual
arousal in females, as well as lifetime pair-bonding of sexual mates
among some species. The chief source of oxytocin in the brain is the
paraventricular nucleus, which resides in a deep-brain structure called
the hypothalamus that serves as a manifold master regulator of body
temperature, hunger, thirst, sleep, emotional reactions and more.
Research over the last 20 to 40 years has suggested that oxytocin
plays a role in promoting not just sexual or nurturing behavior, but
also sociability. A 2013 study
co-authored by Malenka showed that oxytocin was essential to
reinforcing friendly, social behavior in mice. But how that occurred was
unclear, as the paraventricular nucleus sends oxytocin-squirting nerve
tracts to many areas throughout the brain.
So Malenka and his colleagues designed experiments to nail down
oxytocin’s role in social behavior. They confirmed that a tract running
from the paraventricular nucleus to the ventral tegmental area carried
oxytocin. They showed, for the first time, that activity in this tract’s
oxytocin-secreting neurons jumped during mice’s social interactions and
that this neuronal activity was required for their normal social
behavior. Disrupting this activity inhibited sociability but didn’t
impair the mice’s movement or their appetite for pleasurable drugs, such
as cocaine.
The researchers demonstrated that oxytocin secreted in the ventral
tegmental area by neurons originating in the paraventricular nucleus
fosters sociability by binding to receptors on the dopamine-secreting
neurons that compose the tract running from the ventral tegmental area
to the nucleus accumbens, enhancing the firing of the reward-circuit
tract.
The findings should help translational researchers develop
medications for individuals with neurological disorders, such as autism,
depression and schizophrenia, whose conditions compromise their ability
to experience pleasure from connecting with other people, Malenka said.
But he also voiced a desire for more widespread applications of the
research. “With so much hatred and anger in the world,” he said, “what
could possibly be more important than understanding the mechanisms in
the brain that make us want to be friendly with other people?”
This article has been republished from materials provided by Stanford University. Note: material may have been edited for length and content. For further information, please contact the cited source.
