Kyle G. Ratner

Electrophysiological Correlates of Spatial Orienting Towards Angry Faces: A Source Localization Study

The goal of this study was to examine behavioral and electrophysiological correlates of involuntary orienting toward rapidly presented angry faces in non-anxious, healthy adults using a dot-probe task in conjunction with high-density event-related potentials and a distributed source localization technique. Consistent with previous studies, participants showed hypervigilance toward angry faces, as indexed by facilitated response time for validly cued probes following angry faces and an enhanced P1 component. An opposite pattern was found for happy faces suggesting that attention was directed toward the relatively more threatening stimuli within the visual field (neutral faces). Source localization of the P1 effect for angry faces indicated increased activity within the anterior cingulate cortex, possibly reflecting conflict experienced during invalidly cued trials. No modulation of the early C1 component was found for affect or spatial attention. Furthermore, the face-sensitive N170 was not modulated by emotional expression. Results suggest that the earliest modulation of spatial attention by face stimuli is manifested in the P1 component, and provide insights about mechanisms underlying attentional orienting toward cues of threat and social disapproval.

A Memory Systems Model of Implicit Social Cognition

Implicit social cognition refers to the mental processes that influence social perception and behavior independently of conscious awareness. To date, implicit social processes have been explained by single-system models of associations among concepts that, while addressing questions of information processing, are generally silent regarding the interface of implicit social processes with behavior. In this article, we present a multisystem model of implicit social cognition based on emerging cognitive neuroscience research on systems of learning and memory. This model describes how different underlying memory systems, characterized by different patterns of learning, unlearning, and behavioral expression, may contribute to implicit social processes. We describe how the memory systems model differs from previous theories of implicit social cognition and how it makes new and increasingly refined predictions regarding implicit sociocognitive processes and their influences on behavior.

Visualizing Minimal Ingroup and Outgroup Faces: Implications for Impressions, Attitudes, and Behavior

More than 40 years of research have shown that people favor members of their ingroup in their impressions, attitudes, and behaviors. Here, we propose that people also form different mental images of minimal ingroup and outgroup members, and we test the hypothesis that differences in these mental images contribute to the well-established biases that arise from minimal group categorization. In Study 1, participants were assigned to 1 of 2 groups using a classic minimal group paradigm. Next, a reverse correlation image classification procedure was used to create visual renderings of ingroup and outgroup face representations. Subsequently, a 2nd sample naive to the face generation stage rated these faces on a series of trait dimensions. The results indicated that the ingroup face was significantly more likely than the outgroup face to elicit favorable impressions (e.g., trusting, caring, intelligent, attractive). Extending this finding, Study 2 revealed that ingroup face representations elicited more favorable implicitly measured attitudes than did outgroup representations, and Study 3 showed that ingroup faces were trusted more than outgroup faces during an economic game. Finally, Study 4 demonstrated that facial physiognomy associated with trustworthiness more closely resembled the facial structure of the average ingroup than outgroup face representation. Together, these studies suggest that minimal group distinctions can elicit different mental representations, and that this visual bias is sufficient to elicit ingroup favoritism in impressions, attitudes and behaviors.

Perceived Stigmatization, Ingroup Pride, and Immune and Endocrine Activity Evidence From a Community Sample of Black and Latina Women

Racial disparities are a major public health concern in the United States. The authors examined whether Black and Latina community members’ perceptions of stigmatization and personal feelings about their group relate to immune and endocrine markers associated with health risk, including the cytokine interleukin-6 (IL-6), which coordinates the immune response to infection, the anabolic hormone dehydroepiandrosterone (DHEA), which promotes cellular resilience, and the catabolic hormone cortisol, which releases metabolic stores in response to threat. Greater perceived stigmatization was associated with higher basal IL-6, whereas greater ingroup pride was related to elevated basal DHEA. These associations remained with adjustment for general perceived stress, experience with discrimination, age, and income. No significant perceived stigmatization or ingroup pride effects emerged for basal cortisol. These findings provide new evidence that perceived stigmatization and ingroup pride are linked to indicators of disease and resilience, respectively, highlighting mechanisms through which racial and ethnic stigmatization may contribute to health disparities.

Political Attitudes Bias the Mental Representation of a Presidential Candidate’s Face

Using a technique known as reverse-correlation image classification, we demonstrated that the face of Mitt Romney as represented in people’s minds varies as a function of their attitudes toward Mitt Romney. Our findings provide evidence that attitudes bias how people see something as concrete and well learned as the face of a political candidate during an election. Practically, our findings imply that citizens may not merely interpret political information about a candidate to fit their opinion, but also may construct a political world in which they literally see candidates differently.

Genetic contributions to intergroup responses: a cautionary perspective.

We live in an era where genomic informa-tion can be collected with the ease of a saliva sample and the cost of genotyping is plummeting (Hirschhorn and Daly, 2005; Quinque et al., 2006 ). Intergroup research-ers interested in incorporating biologi-cal approaches into their methodological toolbox are thus faced with the question of whether molecular genetics can provide novel insight into their understanding of people’s responses to members of other groups. In the current commentary, we stitch together human and animal neuro-science with insight from molecular biology to posit mechanisms through which genetic variation and life experience may give rise to responses during intergroup situations. We then discuss avenues for empirical inves-tigation and urge for responsible research practices that take into consideration the negative societal consequences that can result from overinterpreting genetic data.Intergroup phenomena, such as dis-crimination and ethnic violence, emerge at the interindividual level, and as a result, cannot be fully explained by intrapsychic processes. However, in order to understand the effects of intergroup influences on the individual, it is useful to examine the pro-cesses unfolding in the person’s mind and brain. For this reason, researchers have increasingly combined experimental social psychology and neuroimaging techniques to dissect the neural basis of affective and cognitive mechanisms that contribute to intergroup responses. This approach has revealed many interconnected, but disso-ciable, brain regions involved in perceiving, evaluating, and regulating behaviors toward other people, including the amygdala, fusi-form gyrus, anterior cingulate cortex, and various parts of the prefrontal cortex. For comprehensive reviews of the existing neu-roscience research pertaining to intergroup relations we direct readers to Amodio and Ratner (2011) , Cunningham and Van Bavel (2009), Ito and Bartholow (2009), and Kubota et al. (2012).To understand how these neuroimag-ing findings might relate to genetics, it is important to recognize that communica-tion between neurons is facilitated by neu-rochemicals, such as neurotransmitters (e.g., serotonin, dopamine), neurotrophic factors (e.g., BDNF), and hormones (e.g., cortisol, testosterone, and oxytocin). The enzymes that synthesize these molecules, the receptors to which they bind, and the reuptake mechanisms and enzymes that determine their availability are all pro-teins that are coded for by genes (Way and Gurbaxani, 2008). Thus, the cellular and molecular levels of analysis, although not currently considered by most intergroup researchers, have the potential to provide unique insight into how genetic variation might influence intergroup responses.Genes are biologically meaningful seg-ments of DNA ( Snyder and Gerstein, 2003 ). Each gene consists of a sequence of nucleo-tides. Frequent variations in the ordering, number, type, and repetition of nucleotides are called polymorphisms. A single gene can have many different types of polymor -phisms (den Dunnen and Antonarakis, 2001; Gibson and Muse, 2002). In order for polymorphisms to influence cellular functioning, their genetic code has to be transcribed into RNA and this RNA needs to be translated into amino acids. The type of amino acids that are produced and their configuration determine the form of the resultant proteins (e.g., enzymes, receptors; Crick, 1958).Gene expression occurs when bio-chemical processes within a cell stimulate transcription factors that bind to particu-lar DNA motifs (i.e., specified nucleotide sequences) in the promoter region of a gene. Extracellular events can control genomic responses through receptor-mediated chan-nels (Cole, 2009). Relevant to the present concerns, social stressors, such as interact-ing with unknown outgroup members, have been shown to elevate levels of the hormone cortisol (Page-Gould et al., 2008; Amodio, 2009). Other research indicates that cor-tisol binds to corticosteroid receptors and then the bound receptors translocate to the nucleus and act as transcription factors. One effect is that they bind to sites in the promoter of the serotonin transporter gene to trigger the synthesis of proteins that con-trol the reuptake of extracellular serotonin. The availability of serotonin has impor-tant effects on an individual’s emotional responses and also indirectly contributes to serotonin regulation by influencing hypo-thalamic–pituitary–adrenal (HPA) path-ways that release cortisol ( Glatz et al., 2003; Heisler et al., 2007; Way and Gurbaxani, 2008). Thus, at the level of gene expression there is a bidirectional relationship between the genetic code and the environment.The expression of a gene can also be influenced by epigenetic factors, such as DNA methylation and histone modification (Goldberg et al., 2007). DNA methylation occurs when a methyl group attaches to the promoter region and blocks DNA transcrip-tion. Environmental factors (e.g., stress) can increase DNA methylation, and thus have long-term effects on gene expression. Research in rodents has shown that DNA methylation can persist through the repro-ductive process, and as a result, can influence

Unselfish genes? The quest to uncover genomic influences on prosocial behavior.

In the current commentary, we discuss Stoltenberg and colleagues’ finding (reported in this issue) that variation in the serotonin transporter gene (5-HTTLPR) is associated with prosocial behavior via effects on anxiety in social situations. We note how their results are consistent with evidence from the psychopharmacological literature and illustrate how a mediational framework can inform understanding of genetic and psychological associations, and we suggest that future studies that manipulate social context could further elucidate the relationship between genes involved in serotonin regulation and prosocial behavior.