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What are the neural mechanisms that determine whether an individual cooperates or competes with another member of his or her species? In other words, what neural mechanisms determine whether perceived social stimuli are assigned a positive or a negative valence by the perceiver, with positive social stimuli activating neural pathways that cause contact seeking behaviors, acceptance, caregiving, and other prosocial behaviors, while negative social stimuli activate pathways that cause avoidance, rejection, competition or even attack (antisocial behaviors)? These questions form the overarching issue of this essay, which focuses on the neurobiological mechanisms that shift an individual away from antisocial behaviors and toward prosocial behaviors.

The human amygdala is critical for social cognition from faces. Here, we review the insights that have been gained from human single neuron recordings on how the human amygdala represents social information, with a focus on emotional faces. We review data that shows that a substantial proportion of amygdala neurons respond to facial stimuli. We identify and describe two distinct populations: whole face neurons and part neurons. The former respond holistically to the presentation of whole faces only whereas the later respond specifically to the presence of the eyes or the mouth. We conclude by summarizing current challenges and next steps.

In broad outline the brain’s subsystems can be understood in terms of specific functionality. This chapter introduces these subsystems and provides and overview of how they work together to provide the brain’s cognitive capabilities. The focus of the chapter is the mammalian forebrain, an elaborate complex of structures that take advantage of phylogenetically earlier brain systems to create explicit programs. Executing current programs is the primary responsibility of the Cortical-Basal Ganglia-Thalamus loop. Creating new programs is handled by the Hippocampus, which interprets new information in terms of deviations form a vast library of existing programs, and the Amygdala, whose circuitry marks a potential programs importance. Numerical rating of marked programs as to importance and risk is achieved with the Hypothalamus’s modulation of neurotransmitters.

The assessment of stimulus novelty is a pre-requisite for many kinds of learning. Here, we summarize research on the representation of novelty-and familiarity by individual neurons in the human MTL. These neurons express single-trial learning, i.e. they change their response after a single response. The response strength of these neurons is continuously related to memory strength. We further describe a study that shows that individual MTL neurons phase-lock to ongoing theta rhythms and that the strength of such phase locking during learning is predictive of later memory strength.

Psychopathy is a disorder marked by reduced empathy/ guild and an increased risk for antisocial behavior, particularly instrumental, goal-directed antisocial behavior. This chapter will consider the basis for the “empathy” deficit in psychopathy and show its selectivity for distress cues. Dysfunction in the amygdala’s response to distress cues will be stressed. Finally, the developmental result of this empathy deficit, a selective impairment in responding appropriately to care-based transgressions (actions that harm others) will be discussed.

Social anxiety disorder (SAD) is conceptualized as an excessive and/or unreasonable fear of situations in which the person’s behavior or appearance might be scrutinized and evaluated. This fear is a consequence of the person’s expectation to be judged negatively, which might lead to embarrassment or humiliation. Typical examples of feared and usually avoided social situations are giving a talk in public, performing other tasks in front of others, and interacting with people in general. Although the existence of SAD as a psychopathological entity has been known for at least 100 years, it was only relatively recently, with the publication of DSM-III in 1980, that SAD (or social phobia) acquired the status of an ‘‘official’’ psychiatric diagnosis. The term social anxiety disorder has been increasingly used instead of social phobia, because it is felt that the use of the former term conveys more strongly the pervasiveness and impairment associated with the condition and that this term will promote better recognition of the disorder and contribute to better differentiation from specific phobia (Liebowitz et al., 2000). Like generalized anxiety disorder, social anxiety disorder is common and controversial. Unlike generalized anxiety disorder, which is described in different ways by different diagnostic criteria and different researchers and clinicians, SAD does not suffer from a ‘‘description problem.’’ It is not particularly difficult to recognize features of SAD; what may be difficult is making sense of these features. Main issues associated with SAD are listed below…. 1. Where are the boundaries of SAD? How well is SAD distinguished from ‘‘normal’’ social anxiety and shyness on one hand, and from severe psychopathology on the other? 2. Is there a danger of ‘‘pathologizing’’ intense social anxiety by labeling it a psychiatric disorder? How can the distress and suffering of people with high levels of social anxiety be acknowledged if they are not given the corresponding diagnostic label? 3. Is SAD a bona fide mental disorder? 4. Can the subtyping scheme (nongeneralized vs. generalized SAD) be supported? 5. Is there a spectrum of social anxiety disorders?

In my three decades of teaching university courses in child development, I have come to know thousands of students, many of whom were parents or who became parents soon after completing my class. I also served on boards of directors and advisory committees for child-care centers, preschools, elementary schools, and parent organizations. And my research continually drew me into classrooms, where for countless hours I observed and recorded preschool and school-age children’s activities, social interactions, and solitary behaviors, in hopes of answering central questions about how they learn. As a byproduct of those experiences, parents repeatedly approached me with concerns about how to foster their child’s development in the early years. Their fervent questions, at times riddled with doubt and anxiety, revealed that creating optimum learning environments for young children at home—and ensuring their access to development-enhancing experiences in child care, preschool, and school—have become mounting parental challenges. Consider the following problematic situations that parents recently raised with me: • Bob and Sharon, parents of a 4-year-old: Our daughter, Lydia, could recite her ABCs and count from 1 to 20 by age 2 1/2. When we looked for a preschool, many programs appeared to do little more than let children play, so we chose one with lots of emphasis on academics. To me, Lydia’s preschool seems like great preparation for kindergarten and first grade, but each morning, Lydia hates to go. Why is Lydia, who’s always been an upbeat, curious child, so unhappy? • Angela, mother of a 4-year-old and 6-year-old: My husband and I have demanding careers and need to bring work home in the evenings. I’ve read that it’s the quality of time we spend with our children that’s important, not the quantity. We try hard to give Victor and Jeannine our undivided attention, but they’re often whiny, demanding, and quarrelsome. Many times we end up sending them to their rooms or letting them watch TV, just to get some peace after a long day. What’s the best way to create quality parent–child time? • Talia, mother of a 7-year-old: My son Anselmo, a first grader, constantly asks us to help him with his homework.

Bonobos and chimpanzees are two closely relates species of the genus Pan, yet they exhibit marked differences in anatomy, behaviour and cognition. For this reason, comparative studies on social behaviour, cognition and brain organization between these two species provide important insights into evolutionary models of human origins. This chapter summarizes studies on socio-communicative competencies and social cognition in chimpanzees and bonobos from the authors’ laboratory in comparison to previous reports. Additionally, recent data on species differences and similarities in brain organization in grey matter volume and distribution is presented. Some preliminary findings on microstructural brain organization such as neuropil space and cellular distribution in key neurotransmitters and neuropeptides involved in social behaviour and cognition is presented. Though these studies are in their infancy, the findings point to potentially important differences in brain organization that may underlie bonobo and chimpanzees’ differences in social behaviour, communication and cognition. Les bonobos et les chimpanzés sont deux espèces du genus Pan prochement liées, néanmoins ils montrent des différences anatomiques, comportementales et cognitives marquées. Pour cette raison, les études comparatives sur le comportement social, la cognition et l’organisation corticale entre ces deux espèces fournissent des idées sur les modèles évolutionnaires des origines humaines. Dans ce chapitre, nous résumons des études sur les compétences socio-communicatives et la cognition sociale chez les chimpanzés et les bonobos de notre laboratoire en comparaison avec des rapports précédents. En plus, nous présentons des données récentes sur les différences et similarités d’organisation corticale du volume et distribution de la matière grise entre espèces. Nous présentons plus de résultats préliminaires sur l’organisation corticale microstructurale comme l’espace neuropile et la division cellulaire dans des neurotransmetteurs clés et les neuropeptides impliqués dans le comportement social et la cognition. Bien que ces études sont dans leur enfance, les résultats montrent des différences d’organisation corticale importantes qui sont à la base des différences de comportement social, la communication et la cognition entre les bonobos et les chimpanzés.