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This chapter examines the evolution of bird brain, social contact, and birdsong. Communicative capabilities are widespread, whether in song or through other forms of intimate social contact. One mechanism for this is the regulation of information molecules in the brain such as vasopressin and oxytocin. The chapter first provides an overview of information molecules before connecting these processes to song in frogs, crickets, and birds. It then considers neurogenesis and how information molecules work in the human brain, focusing on some core biology underlying animal song and social contact. It shows that steroid hormones facilitate neuropeptide expression in many species, which underlies song tied to the regulation of the internal milieu, territorial expression, reproduction, and a much wider range of social behaviors.

In this chapter we provide an overview of recent research on the biopsychological correlates of implicit motives. We review evidence for a role of gonadal steroids (testosterone and estradiol) as well as stress axis activation in power motivation arousal and satisfaction/frustration, summarize recent research on the role of progesterone and affiliation motivation, and discuss a possible role for arginine–vasopressin in achievement motivation. We also present findings from brain imaging work that indicate that the needs for power, affiliation, and achievement modulate activity in a core motivational circuit consisting of striatum, amygdala, orbitofrontal cortex, and insula when nonverbal social incentives are processed.

This chapter orients the reader to the current biological models of delinquent psychopathology and provides an overview of the biological literature; including heritability, psychophysiology, neurobiology, and endocrinology related to the development of persistent criminal behavior in children and adolescents. The four areas of crime-related psychopathology discussed are early-onset conduct disorder, juvenile psychopathy, bullying, and sex offending. Research is presented in connection with widely accepted biological models of behavior. This chapter also highlights the strengths and limitations of the existing literature, consolidates this literature to identify patterns of convergence and divergence across disorders, and suggests areas for future research.

Affiliation motivation, unlike other implicit motives, seems to have a dual nature. There is a bright positive side and a dark negative side to this implicit motive. The former is best captured by Intimacy motivation; the latter by Affiliation motivation. Research and theory supporting this duality is reviewed. These include data on social interaction, hormone profiles and correlates, autobiographical memory, social sensitivity, and leadership. Measurement issues are also reviewed. Basically, affiliation motivation is focused on not being alone and on a fear of rejection. This explains its dark side. Intimacy motivation is focused on close, meaningful, and mutually satisfying interactions. This explains its mostly positive correlates. Work carried out on dependency also shows a positive and negative side to this variable. These results come from a research tradition completely independent of implicit motives and yet parallel the findings concerning affiliation and intimacy very closely. These independent findings therefore provide support for the model. Finally, the results are shown to parallel the phenomenology of affiliation in the real, interpersonal world.

A basic understanding of how endocrine dysfunction affects the central nervous system is important for a majority of cases referred for assessment by clinical neuropsychologists. Beyond playing a role in assessment and management in more obvious scenarios, such as pituitary adenoma and Graves' disease, increasing attention is being paid to the role of neuropsychology in assessment and management of cognitive dysfunction due to illnesses with direct or indirect effects on the endocrine system and, secondarily, the central nervous system. This chapter discusses principal syndromes of the neuroendocrine system, disorders involving the thyroid hormones, diabetes mellitus, disorders involving the reproductive hormones, disorders involving the adrenal hormones, and melatonin.

This chapter explains how psychological stress affects the brain, neuroendocrine system and ultimately, the cardiovascular and immune systems. A theoretical model is presented that details the effects of stress on the locus ceruleus and sympathetic nervous system, which connect the brain to primary and secondary lymph organs. The chapter discusses how stress affects the hypothalamus, the pituitary gland, the adrenal gland, and the hormones produced by these glands which ultimately affect cellular immunity, antibody production and cytokine activity. It also examines how religious beliefs and activity might influence this system by improving coping and increasing support or, alternatively, may simply be a marker for some other factor (genetic or acquired) that is associated with lower stress and greater sociability.

In the search for biological influences on cognition, steroid hormones have proven to be engaging variables in psychological research for over two decades. Hormones have been claimed to influence a variety of cognitive abilities from spatial and verbal abilities to various forms of memory. Hormones and cognition have been compared both within and between men and women. This chapter presents the rationale for studying sex hormones in relation to cognition, and reviews and discusses hormonal influences on cognitive functioning in adulthood and old age. It focuses on the potential role of steroid hormones on sex differences in cognitive function across the adult life span. Testosterone (T), in particular, is examined for its possible influence on spatial abilities in both men and women. The chapter also addresses questions regarding the effect on cognition of endogenous estrogen levels in pre- and postmenopausal women, the contribution of hormone replacement therapy (HRT) on cognition in postmenopausal women, and the potentially protective effect of estrogen for the development of Alzheimer’s disease.

This essay describes neurobiological and neuroendocrine mechanisms that are implicated in human caregiving. Anatomical and biochemical systems that first appeared in the evolutionary transition from reptiles to mammals allowed the emergence of mammalian sociality. Human behaviors are characterized by symbiotic and reciprocal interactions, which are necessary for successful caregiving. The autonomic nervous system, and especially the mammalian changes in the parasympathetic system, provides an essential neural platform for social behavior. Especially critical to coordinating the features of positive sociality are neuropeptides including oxytocin and vasopressin. These neuropeptides modulate the mammalian autonomic nervous system to foster the expression of social behaviors and, when adaptive, defensive behaviors. Oxytocin, the same peptide that regulates various aspects of mammalian reproduction including birth, lactation and maternal behavior, is also involved in the beneficial and reciprocal effects of caregiving on physiology, behavior and health.

Chapter 2 provides an overview of the neural and endocrine mechanisms that govern the timing and onset of puberty (reproductive maturation). The cells and hormones that comprise the hypothalamic–pituitary–gonadal (HPG) axis are introduced, followed by an explanation of how both negative and positive neuroendocrine feedback loops regulate circulating levels of gonadal steroid hormones in males and females. The rest of the chapter is devoted to mechanisms that govern the timing of puberty and activation of the HPG axis at the onset of puberty. The role of the metabolic hormone leptin as a permissive signal for the timing of puberty, the role of neural excitation and disinhibition in the awakening of the gonadotropin-releasing hormone (GnRH) neurons at the onset of puberty, and the role of the neuropeptide kisspeptin as a proximal driver of HPG axis activation are highlighted. Finally, recent research on hierarchical gene networks that are ultimately responsible for the developmental unfolding of activation of GnRH neurons at puberty onset is reviewed.

This chapter describes fear and its neuroendocrine regulation. It specifically highlights the role of elevated cortisol and corticotropin-releasing hormone (CRH) in the regulation of fear responses, placing a particular emphasis on the central nucleus of the amygdala and the bed nucleus of the stria terminalis. It starts with a discussion of the central motive state of fear and its biological basis. It then discusses the neural circuitry that underlies the perception of fearful events and fear-related behaviors. Next, it presents a description of the neuroendocrine basis of fear and a discussion of glucocorticoids and CRH in sustaining fear-related behaviors. Moreover, it evaluates the role of norepinephrine and epinephrine in facilitating responses to and memory of aversive events. It is showed that neuropeptides such as CRH chemically code the sense of fear that is sustained by elevated cortisol and that may underlie the excessively shy, fearful child's hyperexcitable central state.

This chapter explores the influences of hormones on brain development and how these effects have implications for understanding the development of both shyness and disease. It reviews studies of hormone action that illuminate these principles and illustrate the rapidly increasing understanding of the lifelong interactions between genes and environment as they affect the progression toward disease. The data presented display some of the new information indicating that the brain is a plastic and ever-changing organ of the body and is very much influenced by life experiences. It appears very likely that the condition of extreme fear and shyness offers to a lifelong pattern of allostatic load and that structural and functional correlates will be found to exist in the brains of those individuals who are extremely shy and fearful.

This chapter discusses hormones in relation to psychopathy. Hormones are chemical messengers that travel through the bloodstream and bind to receptors in the brain and body. When hormones bind to receptors in the brain, they can affect the functioning of brain regions. Hence, hormones can be thought of as an intermediate step between genetic or environmental factors and brain functioning. In addition, hormone systems are highly sensitive to environmental and psychological factors such as stress. The chapter specifically studies two primary hormones that have been associated with psychopathy—cortisol and testosterone. Cortisol and testosterone have been associated with several features that are observed in psychopathy, including blunted stress reactivity, fearlessness, aggression, and stimulation seeking.

This chapter reviews the basic arguments related to evolutionary claims for music. In particular, it describes the theory of evolution by natural selection. Before entertaining some possible evolutionary views of music's origins, first it considers two pertinent complicating points of views. One view is that music is a form of nonadaptive pleasure seeking (NAPS). A second view is that music is an evolutionary vestige. It then measures the adaptive value of music. Of the various proposals concerning a possible evolutionary origin for music, eight broad theories can be identified: mate selection, social cohesion, group effort, perceptual development, motor skill development, conflict reduction, safe time passing and transgenerational communication. There are four types of evidence considered in presenting a case for the evolutionary origins of music. Next, it reports some of the archaeological, anthropological, and ethological facts. Moreover, it explores some of the evolutionary arguments that have been advanced to account for the origins of language. The evidence on music and social bonding is shown. Furthermore, a discussion on music and social function, social bonding and hormones, oxytocin and the biology of social bonding, and mood regulation is provided.

Chapter 1 provides the context and conceptual framework for the authors’ approach to thinking about the science of puberty and adolescence. The overarching principle is that the transition from childhood to adulthood that occurs during puberty and adolescence involves complex and iterative interactions between the developing brain, hormones, and experience. This chapter first introduces the concepts of puberty and adolescence and discusses how they are separate, yet intricately linked, developmental processes. Examples of how puberty, defined as reproductive maturation, can be dissociated from adolescence, defined as maturation of the cognitive, emotional, and social behaviors associated with adulthood, are discussed. Other examples highlight the recurring interactions between the brain, pubertal hormones, and experience that ultimately result in an adult individual. The chapter then traces the evolution and growth of research on puberty and adolescence during the last half of the 20th century, which started with puberty being studied mainly by endocrinologists and adolescence being studied mainly by psychologists, and progressed to both puberty and adolescence becoming a focus for basic research conducted by psychobiologists and developmental neurobiologists. The advent of magnetic resonance imaging made possible imaging of the human brain in healthy adolescents; this methodological advance led to new knowledge of the scope and timing of adolescent brain development and how it is shaped by pubertal hormones.

This chapter begins with some history of the field of behavioral neuroendocrinology and traces the origins of the classic organizational-activational hypothesis to explain sexual differentiation of the brain and behavior and hormonal influences on sex-typical social behaviors. The classic hypothesis posits that testicular hormones masculinize and defeminize neural circuits during a perinatal sensitive period, programming sex-typical activational responses to gonadal hormones in adulthood. Research since the mid- to late 1980s shows that a second wave of hormone-dependent organization of the brain and behavior occurs during puberty and adolescence and that ovarian hormones are actively involved in feminization of the brain during the adolescent period of organization. Next, a conceptual framework is presented for studying adolescent development of social cognition (the mental processes by which an individual encodes, interprets, and responds to sensory information from an animal of the same species) in the context of social reorientation, when during adolescence the source of social reward shifts from family to peers. The chapter reviews the literature on what social behaviors and aspects of social cognition are organized by pubertal hormones in males, as well as the nonsocial behaviors that are organized by pubertal hormones in males and females.

Chapter 5 describes development as also an “intelligent” process, transforming an original “speck” of matter into bodies and brains of dazzling competencies and varieties, all utilizing a single genome. It starts to tell us how potential and variation are actively created through the system dynamics, rather than passively “received” in genes. A dynamical, “intelligent” physiology, coordinating activities in disparate tissues, also has much to tell us about the nature of individual differences. The chapter begins to show how intelligent systems have evolved at many different levels, corresponding with more changeable environments.

An effort to mitigate the cumbersome physiological, cognitive, and psychological changes that naturally occur during the menopausal transition has been ongoing for decades. Discrepant findings of symptom presentation and mediation across translational models and among human studies have perplexed researchers for years. Specifically, as an understanding of the role of estrogenic signaling in processes underlying cognition and emotion regulation evolved, researchers speculated that exogenous hormonal therapy might modify disease/symptom onset and course. This chapter describes the variable methodological approaches that likely led to disparities in the literature around hormone therapy use, particularly as it pertains to manipulating symptom onset and course of Alzheimer’s pathology. The authors expound upon current recommendations for exogenous hormone therapy use in aging women and how researchers arrived at these conclusions. Finally, we describe remaining questions regarding hormone therapy use and its long-term impact on cognition and mood, Alzheimer’s disease biomarkers, vascular functioning, and genomic variables.

Neuroscience offers insight into processes that support the development of the social brain within the cultural contexts that permit attachment relationships to form. Both human and nonhuman animal studies are critical to inform theory development and hypothesis testing via descriptive and experimental studies. A scientifically valid evolutionary theory is necessary to account for the remarkable diversity of parenting systems across human and many nonhuman animals. This chapter examines the neural foundations of attachment and poses critical questions that relate to the initiation of this relationship: How does attachment interface with brain development? What is the interplay between attachment and brain development (including elements of bidirectionality)? Are there negative consequences associated with variation in attachment, and are they reversible? Rather than conceptualizing attachment in terms of a single type of relationship, or a rigid developmental channel, this chapter proposes that an expanded consideration of variation is necessary to understand the neural foundations of infant-caregiver relationships, and the role of those relationships in developing competence across the life span. This approach will permit identification of common neurobiological elements of attachment as well as the remarkable plasticity and diversity within and across individuals, cultures, and species.

This chapter discusses the pros and cons of using estrogen and cognition-enhancing drugs in treating neuropsychiatric conditions, and presents health risks related to a decrease in estrogen levels in middle-age women, including Alzheimer’s disease, depression, and cognitive impairment. The use of hormone-replacement therapy for women during and after menopause, whose estrogen levels were low, was questioned following the Women’s Health Initiative report of risks and benefits of estrogen replacement. The chapter presents studies on the use of cognition-enhancing drugs by healthy, older individuals. The use of amphetamines to enhance cognition in older people is discussed along with its drawback of being addictive. The chapter discusses the positive effect of caffeine on improving cognition and its impact on the pathology of Alzheimer’s disease.