Janine M. Dutcher

The role of the ventral striatum in inflammatory-induced approach toward support figures

Although considerable research has shown that inflammation leads to social withdrawal more generally, it is also possible that inflammation leads to social approach when it comes to close others. Whereas it may be adaptive to withdraw from strangers when sick, it may be beneficial to seek out close others for assistance, protection, or care when sick. However, this possibility has never been explored in humans nor have the neural substrates of these behavioral changes. Based on the role of the ventral striatum (VS) in responding to: (1) the anticipation of and motivation to approach rewarding outcomes and (2) viewing social support figures, the VS may also be involved in sickness-induced approach toward support figures. Thus, the goal of the present study was to examine whether inflammation leads to a greater desire to approach support figures and greater VS activity to viewing support figures. To examine this, 63 participants received either placebo or low-dose endotoxin, which safely triggers an inflammatory response. Participants reported how much they desired to be around a self-identified support figure, and viewed pictures of that support figure while undergoing an fMRI scan to assess reward-related neural activity. In line with hypotheses, endotoxin (vs. placebo) led participants to report a greater desire to be around their support figure. In addition, endotoxin (vs. placebo) led to greater VS activity to images of support figures (vs. strangers), and greater increases in inflammation (IL-6 levels) were associated with greater increases in VS activity. Together, these results reveal a possible neural mechanism important for sickness-induced social approach and highlight the need for a more nuanced view of changes in social behavior during sickness.

Why It’s Easier to Remember Seeing a Face We Already Know Than One We Don’t Preexisting Memory Representations Facilitate Memory Formation

In two experiments, we provided support for the hypothesis that stimuli with preexisting memory representations (e.g., famous faces) are easier to associate to their encoding context than are stimuli that lack long-term memory representations (e.g., unknown faces). Subjects viewed faces superimposed on different backgrounds (e.g., the Eiffel Tower). Face recognition on a surprise memory test was better when the encoding background was reinstated than when it was swapped with a different background; however, the reinstatement advantage was modulated by how many faces had been seen with a given background, and reinstatement did not improve recognition for unknown faces. The follow-up experiment added a drug intervention that inhibited the ability to form new associations. Context reinstatement did not improve recognition for famous or unknown faces under the influence of the drug. The results suggest that it is easier to associate context to faces that have a preexisting long-term memory representation than to faces that do not.

Self-Affirmation Improves Problem-Solving under Stress

High levels of acute and chronic stress are known to impair problem-solving and creativity on a broad range of tasks. Despite this evidence, we know little about protective factors for mitigating the deleterious effects of stress on problem-solving. Building on previous research showing that self-affirmation can buffer stress, we tested whether an experimental manipulation of self-affirmation improves problem-solving performance in chronically stressed participants. Eighty undergraduates indicated their perceived chronic stress over the previous month and were randomly assigned to either a self-affirmation or control condition. They then completed 30 difficult remote associate problem-solving items under time pressure in front of an evaluator. Results showed that self-affirmation improved problem-solving performance in underperforming chronically stressed individuals. This research suggests a novel means for boosting problem-solving under stress and may have important implications for understanding how self-affirmation boosts academic achievement in school settings.

Why It’s Easier to Remember Seeing a Face We Already Know Than One We Don’t

In two experiments, we provided support for the hypothesis that stimuli with preexisting memory representations (e.g., famous faces) are easier to associate to their encoding context than are stimuli that lack long-term memory representations (e.g., unknown faces). Subjects viewed faces superimposed on different backgrounds (e.g., the Eiffel Tower). Face recognition on a surprise memory test was better when the encoding background was reinstated than when it was swapped with a different background; however, the reinstatement advantage was modulated by how many faces had been seen with a given background, and reinstatement did not improve recognition for unknown faces. The follow-up experiment added a drug intervention that inhibited the ability to form new associations. Context reinstatement did not improve recognition for famous or unknown faces under the influence of the drug. The results suggest that it is easier to associate context to faces that have a preexisting long-term memory representation than to faces that do not.

Vasopressin, but not oxytocin, increases empathic concern among individuals who received higher levels of paternal warmth: A randomized controlled trial

BACKGROUND Empathy improves our ability to communicate in social interactions and motivates prosocial behavior. The neuropeptides arginine vasopressin and oxytocin play key roles in socioemotional processes such as pair bonding and parental care, which suggests that they may be involved in empathic processing. METHODS We investigated how vasopressin and oxytocin affect empathic responding in a randomized, double-blind, placebo controlled, between-subjects study design. We also examined the moderating role of parental warmth, as reported in the early family environment, on empathic responding following vasopressin, oxytocin, or placebo administration. RESULTS Among participants who reported higher levels of paternal warmth (but not maternal warmth), vasopressin (vs. placebo and oxytocin) increased ratings of empathic concern after viewing distressing and uplifting videos. No main or interaction effects were found for individuals who received oxytocin. CONCLUSIONS Vasopressin has a role in enhancing empathy among individuals who received higher levels of paternal warmth. TRIAL REGISTRATION NCT01680718.

Oxytocin, but not vasopressin, impairs social cognitive ability among individuals with higher levels of social anxiety: A randomized controlled trial

Individuals with social anxiety are characterized by a high degree of social sensitivity, which can coincide with impairments in social cognitive functioning (e.g. theory of mind). Oxytocin (OT) and vasopressin (AVP) have been shown to improve social cognition, and OT has been theorized as a potential therapeutic agent for individuals with social anxiety disorder. However, no study has investigated whether these neuropeptides improve social cognitive ability among socially anxious individuals. In a randomized, double-blind, placebo controlled, between-subjects design we investigated whether social anxiety moderated the effects of OT or AVP (vs placebo) on social working memory (i.e. working memory that involves manipulating social information) and non-social working memory. OT vs placebo impaired social working memory accuracy in participants with higher levels of social anxiety. No differences were found for non-social working memory or for AVP vs placebo. Results suggest that OT administration in individuals with higher levels of social anxiety may impair social cognitive functioning. Randomized-controlled trial registration: NCT01680718.

Self-Affirmation Activates the Ventral Striatum A Possible Reward-Related Mechanism for Self-Affirmation

Self-affirmation (reflecting on important personal values) has been shown to have a range of positive effects; however, the neural basis of self-affirmation is not known. Building on studies showing that thinking about self-preferences activates neural reward pathways, we hypothesized that self-affirmation would activate brain reward circuitry during functional MRI (fMRI) studies. In Study 1, with college students, making judgments about important personal values during self-affirmation activated neural reward regions (i.e., ventral striatum), whereas making preference judgments that were not self-relevant did not. Study 2 replicated these results in a community sample, again showing that self-affirmation activated the ventral striatum. These are among the first fMRI studies to identify neural processes during self-affirmation. The findings extend theory by showing that self-affirmation may be rewarding and may provide a first step toward identifying a neural mechanism by which self-affirmation may produce a wide range of beneficial effects.

PT710. Vasopressin increases empathic responding among those high in primary psychopathy

Multiple stressors are intertwined with work, school and living conditions. Finding reasonable strategy to cope up with stresses has become an important issue to the current society. Although an inspiring idea, first proposed by Cassel, suggested that the positive social support could alleviate adverse stress responses, the underlying mechanisms are still uncovered. In the present study, we evaluated the stress-buffering effect of social interactions on a molecular signal related to abnormal behaviors induced by an hour of acute restraint stress in ICR mice. Interestingly, one hour of restraint stress induced the activation of ERK1/2, which was reduced in the stress group subjected to social interaction with conspecific mice. We also examined the effects of social interaction on behavioral changes induced by restraint stress, assessed through forced swimming test, and Y-maze test. The abnormal behaviors in the stress group were normalized by the addition of social interaction with conspecific mice. To specify the roles of ERK1/2 in these stress-induced abnormal behaviors, we investigated stress-induced behaviors and ERK1/2 level in prefrontal cortex using ERK1/2 inhibitors such as rosuvastatin and SL327. Fascinatingly, these ERK1/2 inhibitors rescued abnormal attention behavior and mood behavior. These results suggest that social interactions could alleviate the acute restraint stress-induced behavioral abnormalities in mice, as well as the overt ERK1/2 activation in the medial prefrontal cortex. Moreover, ERK1/2 might be an important target in social buffering effects against stress. PT709 Dopaminergic functions suppress feeding behavior through neuropeptides in the hypothalamus. Naomi Yonemochi, Hoshi University, Japan Abstract Amphetamine and mazindol are known to reduce food intake by affecting the central dopaminergic neurons. However, central dopaminergic functions in the regulation of feeding behavior still remain unclear. The hypothalamus is a key player in the control of food intake. Therefore, it is possible that dopaminergic functions in the hypothalamus regulate feeding behavior. We showed that density of dopamine D1 and D2 receptors was higher in the lateral hypothalamus (LH; hunger center) than in the ventromedial nucleus of hypothalamus (satiety center). Thus, we investigated the role of lateral hypothalamic dopaminergic functions in feeding behavior of mice. Using in vivo microdialysis, we showed that refeeding significantly increased the dopamine level in the LH after 16-hour fasting. Furthermore, the dopamine D1 receptor agonist SKF 38393 injected into the LH significantly decreased food intake of fasted mice. This decrease was abolished by the dopamine D1 receptor antagonist SCH 23390. Injection of the dopamine D2 receptor agonist quinpirole also decreased food intake and this effect was blocked by the dopamine D2 receptor antagonist l-sulpiride. Since the hypothalamus contains orexigenic neuropeptides such as agoutirelated peptide (AgRP), neuropeptide Y (NPY) and orexin and anorexigenic neuropeptides such as α-melanocyte-stimulating hormone (α-MSH), we examined whether dopaminergic functions regulate these neuropeptides. Using RT-PCR, we indicated that SKF 38393 significantly decreased the mRNA levels of AgRP and NPY, whereas quinpirole induced significant reduction in the mRNA level of preproorexin, precursor of orexin, and significantly increase in the mRNA level of proopiomelanocortin, precursor of α-MSH. In conclusion, these results suggest that the stimulation of dopamine D1 receptors inhibits feeding behavior by inhibiting AgRP and NPY neurons and that the stimulation of dopamine D2 receptors inhibits feeding behavior through the inhibition of orexin neurons and the activation of α-MSH neurons.Amphetamine and mazindol are known to reduce food intake by affecting the central dopaminergic neurons. However, central dopaminergic functions in the regulation of feeding behavior still remain unclear. The hypothalamus is a key player in the control of food intake. Therefore, it is possible that dopaminergic functions in the hypothalamus regulate feeding behavior. We showed that density of dopamine D1 and D2 receptors was higher in the lateral hypothalamus (LH; hunger center) than in the ventromedial nucleus of hypothalamus (satiety center). Thus, we investigated the role of lateral hypothalamic dopaminergic functions in feeding behavior of mice. Using in vivo microdialysis, we showed that refeeding significantly increased the dopamine level in the LH after 16-hour fasting. Furthermore, the dopamine D1 receptor agonist SKF 38393 injected into the LH significantly decreased food intake of fasted mice. This decrease was abolished by the dopamine D1 receptor antagonist SCH 23390. Injection of the dopamine D2 receptor agonist quinpirole also decreased food intake and this effect was blocked by the dopamine D2 receptor antagonist l-sulpiride. Since the hypothalamus contains orexigenic neuropeptides such as agoutirelated peptide (AgRP), neuropeptide Y (NPY) and orexin and anorexigenic neuropeptides such as α-melanocyte-stimulating hormone (α-MSH), we examined whether dopaminergic functions regulate these neuropeptides. Using RT-PCR, we indicated that SKF 38393 significantly decreased the mRNA levels of AgRP and NPY, whereas quinpirole induced significant reduction in the mRNA level of preproorexin, precursor of orexin, and significantly increase in the mRNA level of proopiomelanocortin, precursor of α-MSH. In conclusion, these results suggest that the stimulation of dopamine D1 receptors inhibits feeding behavior by inhibiting AgRP and NPY neurons and that the stimulation of dopamine D2 receptors inhibits feeding behavior through the inhibition of orexin neurons and the activation of α-MSH neurons. PT710 Vasopressin increases empathic responding among those high in primary psychopathy Author/Co-authors Jung Hwa Han1, Benjamin A. Tabak2, Meghan L. Meyer3, Elizabeth Castle2, Janine M. Dutcher2, Michael R. Irwin2,4,5,6, Matthew D. Lieberman2,4, and Naomi I. Eisenberger2 1Section of Affect and Neuroscience, Yonsei University College of Medicine 2Department of Psychology, University of California – Los Angeles, CA 3Department of Psychology, Princeton University 4Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine, University of California – Los Angeles, CA 5Cousins Center for Psychoneuroimmunology, David Geffen School of Medicine, University of California – Los Angeles, CA 6Semel Institute for Neuroscience, David Geffen School of Medicine, University of California – Los Angeles, CA Abstract Individuals with high levels of primary psychopathy, which is associated with a reduced tendency to experience negative affect, tend to show a deficiency in experiencing affective empathy, even though cognitive empathy is left intact. Research on the biological processes underlying empathy has focused on the neuropeptides oxytocin and vasopressin due to their roles in mediating a host of social behaviors. To date, most human research has focused on the social effects of oxytocin with far fewer investigating vasopressin. Although vasopressin has often been associated with aggression in animal research, recent findings in humans suggest that vasopressin may increase prosocial behavior. Using a randomized, double-blind, placebo controlled, between-subjects design, we investigated the main effect of intranasal administration of vasopressin compared to placebo on empathic responses – personal distress and empathic concern – in 83 healthy university students (60 female; Mean Age = 20.84, SD = 2.80). In addition, we investigated the moderating role of psychopathy on the effect of vasopressin on empathic responding.Individuals with high levels of primary psychopathy, which is associated with a reduced tendency to experience negative affect, tend to show a deficiency in experiencing affective empathy, even though cognitive empathy is left intact. Research on the biological processes underlying empathy has focused on the neuropeptides oxytocin and vasopressin due to their roles in mediating a host of social behaviors. To date, most human research has focused on the social effects of oxytocin with far fewer investigating vasopressin. Although vasopressin has often been associated with aggression in animal research, recent findings in humans suggest that vasopressin may increase prosocial behavior. Using a randomized, double-blind, placebo controlled, between-subjects design, we investigated the main effect of intranasal administration of vasopressin compared to placebo on empathic responses – personal distress and empathic concern – in 83 healthy university students (60 female; Mean Age = 20.84, SD = 2.80). In addition, we investigated the moderating role of psychopathy on the effect of vasopressin on empathic responding.