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This chapter summarizes studies examining the link between drugs of abuse and the behavioral neurobiology of aggressive behavior in animal models. It considers studies examining how drug abuse affects the aggressive response patterns of animals, as well as the development, activity, and function of neural systems implicated in aggression control. It shows that the effects of many commonly abused drugs, illegal and prescribed, on aggression are dependent upon the sex and species of the animal, the dosing and treatment regimen, and the behavioral testing paradigm. Although very few drugs, or drug classes, have been shown to consistently influence aggressive behavior regardless of the aforementioned factors (i.e., species, age, sex, dosing, testing paradigm), there are notable exceptions, including some anabolic androgenic steroids (AAS), nicotine, 3,4-methylenedioxymethamphetamine (MDMA), and mescaline. The administration of various types of AAS has consistently increased aggression in various animal species of varying ages regardless of experimental paradigm, whereas nicotine, MDMA, and mescaline have been shown to consistently decrease aggressive responding.

This chapter summarizes the evidence describing the roles that monoamines—5-hydroxytryptamine (5-HT), norepinephrine (NE), and dopamine (DA)—exert in the mediation of aggressive behavior. Aggression is diverse in its behavioral patterns and functions, and endogenous amines, acids, steroids, and peptides may have different effects on each kind of aggression. The importance of escalated forms of aggression is highlighted in an effort to model the harmful acts of aggression and violence in humans. Monoamines have powerful modulatory effects on aggression, and reciprocally, aggression alters monoamines. It is important to delineate the specific conditions and behaviors—when 5-HT appears to be inhibitory, and when NE and DA are aggression stimulating. The effects of monoamines are likely to be due to their interactions with other neurotransmitters, such as gamma-aminobutyric acid (GABA) and glutamate, and neuropeptides, such as vasopressin and opioids.

This chapter discusses the association between drugs and human aggression, laboratory studies of human aggression, and effects of drugs on human aggression under laboratory conditions. It argues that methodological difficulties often prevent unequivocal interpretations of the outcomes of pharmacological treatments of aggression. Conducting well-designed placebo-controlled studies in an inpatient setting is difficult, as drug-free washout periods may be unsafe for both patients and staff. Thus, it is clinically difficult to assess whether a reduction in aggression is a specific effect of the pharmacological agent or of nonspecific effects of medications such as neuroleptics and benzodiazepines commonly used for the management of specific Axis I and Axis II disorders. Nonpharmacological factors, such as the therapeutic milieu, can affect treatment outcome and should be considered when evaluating the efficacy of a pharmacotherapeutic intervention for aggression.

This chapter begins with a brief discussion of the factors that make crustaceans an excellent model for the study of aggressive behavior. It then discusses the natural contexts of aggression, aggression in development, aggressive behavior, dominance hierarchy formation, hormonal control of aggressive behavior, and neural mechanisms of aggressive behavior.

At least two types of estrogen receptors (ERs), the classical ER-α and the more recently identified ER-β, have been localized in the central nervous system. ER-α and ER-β are very similar estrogen binding proteins that act as ligand-dependent transcription factors. Although somewhat overlapping, brain distributions of ER-α and ER-β are not identical. This chapter summarizes current knowledge of the possible differential roles played by the two types of ERs in the expression of aggressive behavior. It also discusses potential brain mechanisms of ER-mediated regulation of aggression.

This chapter begins by discussing the types and contexts of vertebrate aggression and how it is controlled by the endocrine system. It then addresses hormone-aggression interactions and their possible evolution. The chapter shows that various types of aggression can be expressed in multiple contexts, both narrow and broad, throughout the life cycle of an individual. In most species the behavioral traits associated with aggression, both defensive and offensive, are similar regardless of stage in the life cycle. This suggests that neural circuits may indeed be conserved, but the mechanisms by which hormones regulate expression of aggression may vary.

This chapter begins with a discussion of the development of agonistic behavior in mammals. It then discusses the adaptive value of play and play fighting, sex differences and hormonal control of play fighting, neural control of play fighting, and controlling the time course of the maturation of agonistic behavior. It shows a correlation between that maturation of aggressive behavior and maturation of the the hypothalamic-pituitary-adrenal axis (HPA). The HPA axis controls the maturation of aggressive behavior during puberty. It is also likely that adrenarche, the onset of the activity of the HPA axis, controls the appearance of aggressive responses before puberty. This regulation mechanism may provide an explanation for interactions between genes and the environment, as the activity of the HPA axis differs between individuals and can be affected by external stimuli, such as stress.

This chapter reviews the effects of nitric oxide (NO) on aggressive behavior. Topics discussed include NO and aggression in Down syndrome and affective disorders, interaction with serotonin, interaction with the hypothalamic-pituitary-adrenal (HPA) axis, and environmental contributions to NO-mediated aggression.

This chapter focuses on two neurochemical signals that control aggression—serotonin (5-hydroxytryptamine, or 5-HT) and vasopressin (VP). 5-HT and VP appear to play significant roles in the regulation of impulsivity and aggression. 5-HT reduces aggressive responding, while VP enhances arousal and aggression in a context-dependent manner. The interaction between the brain and the environment is regulated, in part, by changes in gonadal and adrenal steroids. The stress of social subjugation alters the levels of testosterone and stress hormones, affecting gene transcription and translation. The VP/5-HT systems are sensitive to changes in these steroid hormones linking the neurochemical regulation of aggression to environmental events.

This chapter begins with a discussion of maternal aggression in rodents and the hormones that affect it. It then discusses the sensory control and neural circuitry of maternal aggression, similarities and differences in the neural control of maternal and intermale aggression, and relationship of fear and anxiety during lactation with maternal aggression.

This chapter explores the nature of media violence and its particular influence on adolescents and their development. It shows the immense power the media potentially plays in adolescent development, including the power not only to shape aggressive and violent dispositions but also to address violence and foster non-violent relationships. To introduce the media's socializing force, the chapter also pays attention to factors that moderate and mediate media effects, although research only recently has turned to these considerations. That is, it considers the factors that shape how the media influences adolescents, since the media does not act alone. Together, findings reveal the need to reconsider how best to prepare adolescents to respond to violent media.

This chapter presents an overview of human quantitative genetic studies of aggression and violence, including twin, adoption, and molecular genetic designs from both the child and adult literature. It begins with the behavioral genetic literature on aggression in childhood and early adolescence. It highlights systematic differences across studies based on the method of assessing aggression, as well as presents evidence for both distinct and common etiologies that link aggression with other childhood behavioral problems. It then considers relevant behavioral genetic investigations of aggression in adulthood. The chapter discusses predominant theories and empirical findings from longitudinal studies of aggression during both childhood and adulthood, as well as highlighting various moderating effects on the etiology of these behaviors (i.e., gender differences and gene-environment interactions). Finally, future directions for behavioral genetic research on aggression are discussed and important domains that have received comparatively less attention in this literature are underscored.

This chapter utilizes conspecific, offensive aggression in males and females as model systems to exemplify androgenic influences on aggressive behavior. This form of aggression is a productive behavior exhibited between same-sex conspecifics; its effects are reflected in dominance status and access to resources.

This chapter reviews neurobiological risk factors for aggression in children. It begins by considering two general positions that have received considerable attention with respect to aggression in children: the frontal lobe and fear dysfunction positions. It then considers a fundamental difficulty with these types of general account of aggression in children—that they implicitly assume all aggression is mediated by the same neural architecture. It argues that a distinction must be made between reactive and instrumental aggression. The neurobiological risk factors for reactive and instrumental aggression are discussed.

This chapter discusses hormonal influences on human aggression. It argues that there is little, if any, evidence supporting contributions of circulating levels of androgens in adulthood to human aggression or to psychological characteristics, like anger and dominance, thought to be associated with aggression. Despite some evidence that prenatal androgen exposure relates to subsequent aggressive response tendencies, studies to date have relied on small samples and have not always produced consistent results. If a link between androgen and aggression receives more convincing empirical support, future research might also investigate the mechanisms underlying this association.

This chapter reviews the major psychophysiological findings and theories regarding antisocial behavior, with a specific focus on skin conductance (SC), heart rate (HR), electroencephalogram (EEG), and startle blink research. Psychophysiological findings in relation to antisocial behavior support the notion that chronic serious antisocial behavior is a disorder that partly arises from a biological dysfunction within the individual. The strongest evidence suggests that antisocial individuals are characterized by fearlessness or emotional detachment, reflected in reduced levels of tonic autonomic (i.e., HR and SC) arousal, increased heart rate variability (HRV), greater slow-wave EEG activity, and reduced startle blink potentiation to unpleasant stimuli. There is also growing evidence of other antisocial behavior characterized more by defensiveness, stress reactivity, and negative emotionality as reflected in decreased HRV, increased SC reactivity, normal or increased affective startle modulation, and left frontotemporal dysfunction.

430 third- to fifth-grade children were followed across a school year to see whether children who play more violent video games early in the school year have changed to become more aggressive by the end of the school year. Researchers measured the children themselves, their peers, and their teachers. They found that both the amount and content of video games matter. The amount of game play was a significant predictor of later poor school performance. Playing violent games increased hostile attribution bias (perceiving the world as a mean place), increased verbal and physical aggression, and decreased pro-social behaviors (as measured by peers and teachers). The effects were reduced (but not eliminated) if parents set limits on the amount and content of screen media for their children.

This chapter presents the General Aggression Model in detail, and shows how it can be used to understand developmental processes and a risk and resilience approach to human aggression. Briefly, the model shows how factors in the immediate situation (such as being insulted while in front of friends, and having just played a violent video game) combine with factors that people bring with them to the situation (such as positive attitudes towards using aggression, impulsive personality, and a habit of taking slights too personally) to produce an internal set of aggression-related thoughts and feelings that are likely to yield aggressive behavior. The model also shows how repeated life experiences of a variety of kinds can lead to the development of an aggressive personality. The chapter concludes with a section on how the General Aggression Model can be used to understand and predict effects of media violence on the development of aggressive behavior and aggressive personality.

This chapter examines the influence of sociopsychosocial factors in aggressive behaviour. It highlights the role of respondent and operating conditioning in the acquisition and elimination of aggression. It discusses attempts to apply the social leaning theory and social learning principles in determining how aggressive behaviours can be controlled by authority figures, non-aggressive models, cognitive manipulations, and incompatible environments. Some of these results may be useful in the development of treatment techniques for aggression.

Media violence and its effects on aggression is one of the most heavily investigated topics in the field of communication. Every time a child or teenager committed an act of violence in recent years, the debate about the effects of media violence on aggression flared up again. Can children and teens indeed become aggressive, or even criminal, from seeing violence on television, in movies, or in games? And if so, are some children and teens particularly vulnerable to media violence effects? This chapter reviews the latest findings on the effects of media violence on aggression and criminal behavior. It first discusses key studies that investigated the effects of media violence on aggression. It then discusses the most important theories of why and how media violence may stimulate aggression. Finally, it reflects on how and why some children may be more—and others less—susceptible to media violence effects.