Vasopressin increases human risky cooperative behavior.

The history of humankind is an epic of cooperation, which is ubiquitous across societies and increasing in scale. Much human cooperation occurs where it is risky to cooperate for mutual benefit because successful cooperation depends on a sufficient level of cooperation by others. Here we show that arginine vasopressin (AVP), a neuropeptide that mediates complex mammalian social behaviors such as pair bonding, social recognition and aggression causally increases humans' willingness to engage in risky, mutually beneficial cooperation. In two double-blind experiments, male participants received either AVP or placebo intranasally and made decisions with financial consequences in the "Stag hunt" cooperation game. AVP increases humans' willingness to cooperate. That increase is not due to an increase in the general willingness to bear risks or to altruistically help others. Using functional brain imaging, we show that, when subjects make the risky Stag choice, AVP down-regulates the BOLD signal in the left dorsolateral prefrontal cortex (dlPFC), a risk-integration region, and increases the left dlPFC functional connectivity with the ventral pallidum, an AVP receptor-rich region previously associated with AVP-mediated social reward processing in mammals. These findings show a previously unidentified causal role for AVP in social approach behavior in humans, as established by animal research.

Older adults show a reduced tendency to engage in context-dependent decision biases.

When we make decisions, we usually consider the context. This can sometimes lead to suboptimal choices or choice abnormalities. One such abnormality is the compromise effect, according to which deciders tend to favour options positioned as a compromise in an available set of extreme options. Theoretical accounts consider that these effects relate to available cognitive resources, which, in turn, have been found to depend on an individual's dopaminergic innervation. Referring to a correlative triad between cognition, dopamine and aging, the present study demonstrates that the compromise effect is replicable in a group of younger adults (n = 27, 20-32 years of age) yet is attenuated in older adults (n = 27, 62-80 years of age). Results from an [18F]-FDOPA-PET analysis in older adults indicate a positive association between older adults' inclination to engage in compromise effects and their striatal dopamine synthesis capacity. These results demonstrate altered context-dependent decision biases in older adults and suggest a neuromodulatory mechanism underlying this irregular choice.

Winning is not enough: ventral striatum connectivity during physical aggression.

Social neuroscience studies have shown that the ventral striatum (VS), a highly reward-sensitive brain area, is activated when participants win competitive tasks. However, in these settings winning often entails both avoiding punishment and punishing the opponent. It is thus unclear whether the rewarding properties of winning are mainly associated to punishment avoidance, or if punishing the opponent can be additionally gratifying. In the present paper we explored the neurophysiological correlates of each outcome, aiming to better understand the development of aggression episodes. We previously introduced a competitive reaction time task that separates both effects: in half of the won trials, participants can physically punish their opponent (active trials), whereas in the other half they can only avoid a punishment (passive trials). We performed functional connectivity analysis seeded in the VS to test for differential network interactions in active compared to passive trials. The VS showed greater connectivity with areas involved in reward valuation (orbitofrontal cortex), arousal (dorsal thalamus and posterior insula), attention (inferior occipital gyrus), and motor control (supplementary motor area) in active compared to passive trials, whereas connectivity between the VS and the inferior frontal gyrus decreased. Interindividual variability in connectivity strength between VS and posterior insula was related to aggressive behavior, whereas connectivity between VS and supplementary motor area was related to faster reaction times in active trials. Our results suggest that punishing a provoking opponent when winning might adaptively favor a "competitive state" in the course of an aggressive interaction.

Vasopressin modulates neural responses related to emotional stimuli in the right amygdala.

The neuropeptide vasopressin has been shown to modulate social and affective processes. Using fMRI we investigated the influence of intranasal vasopressin (AVP) on neural activations related to social cognitions and emotion processing in a group of healthy young men. In a double-blind, placebo controlled between groups design, 20 IU AVP were administered intranasally to half of the participants before scanning, while the other half received saline intranasally. All participants viewed line drawings depicting either one or two persons (social factor) in an emotionally neutral or negative scene (emotional factor). Vasopressin modulated the activation of the right amygdala related to the emotional component of empathy. Moreover, vasopressin also increased connectivity of the right amygdala with the medial prefrontal cortex (mPFC) and the inferior parietal lobule during the processing of pictures illustrating a socially threatening scene. This suggests that AVP reduces suppressive effects of the mPFC on amygdala activity resulting in the observed enhanced neural pattern in the amygdala. At present, it remains unclear whether the increased amygdala activity reflects a direct impact of AVP on vasopressin V1 receptors in the amygdala or an indirect effect via vasopressin V1 receptors in the mPFC or other remote brain sites.

Vasopressin modulates neural responses during human reactive aggression.

The neuropeptide arginine vasopressin (AVP) is known to modulate aggressive behavior in mammals, but the neural mechanisms underlying this modulation are not clear yet. In the present study, we administered 20 IU AVP nasally in a randomized, placebo-controlled, double-blind manner to 36 healthy men using a between-subjects design. After drug administration, participants performed a competitive reaction time task (Taylor Aggression Paradigm, TAP) to elicit reactive aggressive behavior while functional magnetic resonance imaging was recorded. Under AVP treatment, we found increased activations in the right superior temporal sulcus in the decision phase during trials in which participants could get punished after losing the reaction time competition. At the behavioral level, no differences could be found between AVP treatment and placebo condition. The lack of AVP-related behavioral effects is discussed in terms of the general aggression model (GAM).