The Institutional Stance.

Human success in navigating the social world is typically attributed to our capacity to represent other minds—a mentalistic stance. We argue that humans are endowed with a second equally powerful intuitive theory: an institutional stance. In contrast to the mentalistic stance, which helps us predict and explain unconstrained behavior via unobservable mental states, the institutional stance interprets social interactions in terms of role-based structures that constrain and regulate behavior via rule-like behavioral expectations. We argue that this stance is supported by a generative grammar that builds structured models of social collectives, enabling people to rapidly infer, track, and manipulate the social world. The institutional stance emerges early in development and its precursors can be traced across social species, but its full-fledged generative capacity is uniquely human. Once in place, the ability to reason about institutional structures takes on a causal role, allowing people to create and modify social structures, supporting new forms of institutional life. Human social cognition is best understood as an interplay between a system for representing the unconstrained behavior of individuals in terms of minds and a system for representing the constrained behavior of social collectives in terms of institutional structures composed of interlocking sets of roles.

A proposal that human social cognition would not have evolved without mechanisms and practices that shape minds in ways that make them easier to interpret. In this novel account of distinctively human social cognition, Tadeusz Zawidzki argues that the key distinction between human and nonhuman social cognition consists in our complex, diverse, and flexible capacities to shape each other's minds in ways that make them easier to interpret. Zawidzki proposes that such "mindshaping"—which takes the form of capacities and practices such as sophisticated imitation, pedagogy, conformity to norms, and narrative self-constitution—is the most important component of human social cognition. Without it, he argues, none of the other components of what he terms the "human sociocognitive syndrome," including sophisticated language, cooperation, and sophisticated "mindreading," would be possible. Challenging the dominant view that sophisticated mindreading—especially propositional attitude attribution—is the key evolutionary innovation behind distinctively human social cognition, Zawidzki contends that the capacity to attribute such mental states depends on the evolution of mindshaping practices. Propositional attitude attribution, he argues, is likely to be unreliable unless most of us are shaped to have similar kinds of propositional attitudes in similar circumstances. Motivations to mindshape, selected to make sophisticated cooperation possible, combine with low-level mindreading abilities that we share with nonhuman species to make it easier for humans to interpret and anticipate each other's behavior. Eventually, this led, in human prehistory, to the capacity to attribute full-blown propositional attitudes accurately—a capacity that is parasitic, in phylogeny and today, on prior capacities to shape minds. Bringing together findings from developmental psychology, comparative psychology, evolutionary psychology, and philosophy of psychology, Zawidzki offers a strikingly original framework for understanding human social cognition. Bradford Books imprint

In non-human mammals, the neuropeptide oxytocin is a key mediator of complex emotional and social behaviors, including attachment, social recognition, and aggression. Oxytocin reduces anxiety and impacts on fear conditioning and extinction. Recently, oxytocin administration in humans was shown to increase trust, suggesting involvement of the amygdala, a central component of the neurocircuitry of fear and social cognition that has been linked to trust and highly expresses oxytocin receptors in many mammals. However, no human data on the effects of this peptide on brain function were available. Here, we show that human amygdala function is strongly modulated by oxytocin. We used functional magnetic resonance imaging to image amygdala activation by fear-inducing visual stimuli in 15 healthy males after double-blind crossover intranasal application of placebo or oxytocin. Compared with placebo, oxytocin potently reduced activation of the amygdala and reduced coupling of the amygdala to brainstem regions implicated in autonomic and behavioral manifestations of fear. Our results indicate a neural mechanism for the effects of oxytocin in social cognition in the human brain and provide a methodology and rationale for exploring therapeutic strategies in disorders in which abnormal amygdala function has been implicated, such as social phobia or autism.

Human social cognitive abilities share derived attributes with other primates, but humans excel uniquely with regard to skills such as theory of mind, perspective-taking, sharing intentions and using language. Even these apparently unique abilities, however, must be supported by neurochemistry that is in turn developmentally dependent on genes derived from our primate lineage. In the last decade, epigenetic processes have emerged as an influence on differences both within and between mammalian species, and the brain is a major target for epigenetic processes regulating gene expression. This short review looks at how epigenetic processes may have contributed to human social cognitive evolution, how this relates to differences between human and non-human primate social cognition and to what extent this is consistent with the social brain hypothesis, i.e. increasing human sociality as a driver rather than a consequence of human brain evolution. The evidence ranges from general trends in maternally and paternally expressed genes influencing different parts of the brain, quantitative differences in mechanisms such as DNA methylation and gene expression in the brains of humans and other primates and examples of species-specific epigenetic regulation of genes associated with social cognition and language.

Much empirical research on human social cognition and its development pertains to questions of how individuals understand their conspecifics in a causal-descriptive sense, that is, how they explain and predict others’ observable (behavioral) and unobservable (mental) states (e.g., epistemic or volitional states). Human social cognition, however, also entails normativity—the sense of right and wrong—in thought and action. This chapter introduces the notion of normativity and reviews developmental research on the early ontogeny of understanding, learning, and applying different types of normative phenomena (focusing on practical norms, e.g., conventional and moral norms). We report evidence that even very young children engage in rational and selective third-party norm enforcement, which suggests that they understand some important features of normativity (e.g., normative force and generality). Thus, from early on, human social cognition is not only concerned with the prediction and explanation of others’ behavior, but also with the prescription and evaluation of others’ actions—a conceptual space of reasons grounded in a psychological space of shared and collective intentionality.

Imagination in human social cognition, autism, and psychotic-affective conditions

The capacity to understand and reason about the unobservable mental states (e.g., thoughts, desires, and beliefs) of oneself and others, known as theory of mind ( ToM ), is central to human social cognition. Multidisciplinary interest in ToM stems from its potentially unique human nature, the role it plays in our ability to engage in complex social interactions, and its impairment in psychiatric and developmental disorders, such as autism. Through more than 30 years of research, we have learned a great deal about how and when children come to reason about others in terms of their mental states. This essay reviews foundational research on the development of ToM reasoning during childhood; outlines cutting‐edge findings on the infant origins and neural correlates of ToM; and finally discusses key issues for future research, including reconciling infant competence with evidence of protracted conceptual development in early childhood, expanding our neuroscientific understanding of ToM and its development, and shedding light on the use and individual variability of ToM in everyday life. Pursuing these goals will address important theoretical questions and provide critical new insight into the origins, development, neural basis, and social and behavioral consequences of ToM.

Humans readily adopt an intentional stance to other people, comprehending their behavior as guided by unobservable mental states such as belief, desire, and intention. We used fMRI in healthy adults to test the hypothesis that this stance is primed by the default mode of human brain function present when the mind is at rest. We report three findings that support this hypothesis. First, brain regions activated by actively adopting an intentional rather than nonintentional stance to a social stimulus were anatomically similar to those demonstrating default responses to fixation baseline in the same task. Second, moment-to-moment variation in default activity during fixation in the dorsomedial PFC was related to the ease with which participants applied an intentional--but not nonintentional--stance to a social stimulus presented moments later. Finally, individuals who showed stronger dorsomedial PFC activity at baseline in a separate task were generally more efficient when adopting the intentional stance and reported having greater social skills. These results identify a biological basis for the human tendency to adopt the intentional stance. More broadly, they suggest that the brain's default mode of function may have evolved, in part, as a response to life in a social world.

118 Social cognition refers to the whole “mental operation underlying social interactions, which includes the human ability to perceive the intentions and disposition of others” (Brothers, 1990). Although social cognition has differently been defined, most of the researchers suggest that it is composed by the following domains: (a) emotional processing, (b) theory of mind (the ability to infer the intentions and beliefs of others), (c) social perception (which expresses the person’s ability to ascertain social cues from behaviour provided in a social context, including emotional cues), (d) social context, (e) social knowledge (the awareness of the roles, rules and goals that characterize social situations and guides social interactions), and (e) attributional bias (how one explains the causes for positive and negative outcome of events) (Green et al., 2005; Salovey et al., 1997; Toomey et al., 1997). All these dimensions would together support the complex behaviours necessary for social interactions and a neural network involving prefrontal cortex (PFC) areas (i.e. orbitofrontal cortex, ventrolateral, dorsolateral and dorsomedial PFC), cingulate, fusiform gyrus, amygdala, and superior temporal sulcus participate in supporting social cognition in humans (Burns, 2006; Grady et al., 2002). In this regard, individuals with PFC damage have impaired social behaviour and functioning, despite the retention of intact cognitive skills. This would lead to misinterpretation of social situations, especially when the damage is located in the orbitofrontal/ventromedial PFC region (Shamay-Tsoory et al., 2007). Impairment in social functioning is also a core feature of schizophrenia (Spauwen et al., 2006; Pinkham et al., 2003). Burns (2006) argued that the patient’s sense of detachment and disembodiment from “social self” and “social world” is the essential disturbance of schizophrenia. Altered social cognition is in fact present throughout the course of the illness, worsens with chronicity, is often resistant to antipsychotic treatment, and may represent a risk factor for the disease (Killackey et al., 2007; Pinkham et al., 2003; Addington et al., 2000). Moreover, since social cognition partially sustains functioning, it is considered an intervention target (Green et al., 2008) and some studies have shown that cognitive training may improve social outcome measures in schizophrenia (Combs et al., 2007; Jabben et al., 2007; Wolwer et al., 2005). Indeed, there is growing evidence that social cogAddress for correspondence: Dr. M. Bellani, Department of Medicine and Public Health, Section of Psychiatry and Clinical Psychology, University of Verona, Piazzale L.A. Scuro 10, 37134 Verona (Italy). Fax: +39-045-585.871 E-mail: marcella.bellani@univr.it Social cognition, schizophrenia and brain imaging

According to the organizational-activational hypothesis, the organizational effects of testosterone during (prenatal) brain development moderate the activational effects of adult testosterone on behavior. Accumulating evidence supports the notion that adolescence is another period during which sex hormones organize the nervous system. Here we investigate how pubertal sex hormones moderate the activational effects of adult sex hormones on social cognition in humans. To do so, we recruited a sample of young men (n = 507; age, ∼19 years) from a longitudinal birth cohort and investigated whether testosterone exposure during adolescence (from 9 to 17 years of age) moderates the relation between current testosterone and brain response to faces in young adulthood, as assessed with functional magnetic resonance imaging (fMRI). Our results showed that the cumulative exposure to testosterone during adolescence moderated the relation between adult testosterone and both the mean fMRI response and functional connectivity (i.e., node strength). Specifically, in participants with low exposure to testosterone during puberty, we observed a positive relationship between current testosterone and the brain response to faces; this was not the case for participants with medium and high pubertal testosterone. Furthermore, we observed a stronger relationship between the brain response and current testosterone in parts of the angry-face network associated with (vs without) motion in the eye region of an observed (angry) face. We speculate that pubertal testosterone modulates the relationship between current testosterone and brain response to social cues carried by the eyes and signaling a potential threat.SIGNIFICANCE STATEMENT Accumulating evidence supports the organizational effects of pubertal testosterone, but the body of literature examining these effects on social cognition in humans is in its infancy. With a sample of young men from a longitudinal birth cohort, we showed that the cumulative exposure to testosterone during adolescence moderated the relation between adult testosterone and both the mean BOLD signal change and functional connectivity. Specifically, we observed a positive relationship between adult testosterone and the brain response to faces in participants with low exposure to testosterone during puberty, but not in participants with medium and high pubertal testosterone. Results of further analysis suggest that sensitivity to cues carried by the eyes might underlie the relationship between testosterone and brain response to faces, especially in the context of a potential threat.

Exploring the evolutionary roots of theory of mind: Primate errors on false belief tasks reveal representational limits.

Learning from other minds: an optimistic critique of reinforcement learning models of social learning

Prelims

We focus in this chapter on the human social cognitive ability to connect with each other at the level of dierent inner and unobservable mental states such as knowledge and beliefs; a development encapsulated in the term theory of mind (ToM). The development of children’s ToM has been a major research topic for the last 30 years and recently attention has turned to the environmental enablers of social cognition found in early parent-child interaction.

The neurohormone oxytocin plays a central role in human social behaviour and cognition, and oxytocin dysregulation may contribute to psychiatric disorders. However, genetic factors influencing individual variation in the oxytocinergic system remain poorly understood. We genotyped 169 healthy adults for a functional polymorphism in GTF2I ( general transcription factor II-I ), a gene associated with high prosociality and reduced social anxiety in Williams syndrome, a condition reported to involve high oxytocin levels and reactivity. Participants’ salivary oxytocin levels were measured before and after watching a validated empathy-inducing video. Oxytocin reactivity, defined as pre- to post-video percentage change in salivary oxytocin, varied substantially and significantly between individuals with different GTF2I genotypes, with, additionally, a trend towards an interaction between genotype and sex. Individuals with more oxytocin-reactive genotypes also reported significantly lower social anxiety. These findings suggest a model whereby GTF2I has a continuum of effects on human sociality, from the extreme social phenotypes and oxytocin dysregulation associated with gene deletion in Williams syndrome, to individual differences in oxytocin reactivity and sociality associated with common polymorphisms in healthy populations.