From their early roots in embryology, parallels are drawn between the major psychological and biological foci of organismic theories. Neural plasticity and concepts of causality in developmental systems are discussed. Because the nature of the developmental process necessitates addressing the nonlinear dynamics of complex systems, it is theorized that causal explanations in neural development, just as is the case with psychological processes, should emphasize the individual's active strivings for self-organization as the major determinant of ontogenesis. Whether or not they cohere to form an integrated self, it is hypothesized that the homeostatic, self-regulatory structures of the mind are the major stabilities in the chaotic dynamics of psychological and neural development.

Parcellation and heterochrony (neoteny) reflect the pattern and rate of a growth mechanism in morphogenesis. Structure (morphology) and function (behavior) are staged realizations of morphogenetic process. This process continues into adult cognition in the actualization of the mind/brain state. Parcellation obtains in the pruning of cells and connections in early growth, whereas inhibition obtains in a relatively stable morphology with constraints on context: item transforms in microgeny. Selective retardation in process (neoteny) leads to growth at earlier (juvenile) phases. This accounts for the specification of the language areas and elaboration at preliminary phases in mind — for example, dominance, introspection, and creativity.

A new theory of frontal lobe development is presented in which the role of the human frontal lobes during normal development and the psychopathological consequences of early frontal lobe injury are explored. Analyses of the development of human electroencephalograph (EEG) coherence indicate that there are oscillations and cyclic growth processes along the mediolateral and anterior-posterior planes of the brain. The cycles of EEG coherence are interpreted as repetitive sequences of increasing and decreasing synaptic effectiveness that reflects a convergence process that narrows the disparity between structure and function by slowly sculpting and reshaping the brain's microanatomy. This process is modeled as a developmental spiral staircase in which brain structures are periodically revisited resulting in stepwise increases in differentiation and integration. The frontal lobes play a crucial role because they are largely responsible for the selection and pruning of synaptic contacts throughout the postnatal period. A mathematical model of cycles of synaptic effectiveness is presented in which the frontal lobes behave as gentle synaptic “predators” whereas posterior cortical regions behave as synaptic “prey” in a periodic reorganization process. The psychopathological consequences of early frontal lobe damage are discussed in the context of this model.

Disorders of emotion, communication, and learning in early childhood are considered in light of evidence on human brain growth from embryo stages. We cite microbehavioral evidence indicating that infants are born able to express the internal activity of their brains, including dynamic “motive states” that drive learning. Infant expressions stimulate the development of imitative and reciprocal relations with corresponding dynamic brain states of caregivers. The infant's mind must have an “innate self-with-other representation” of the inter-mind correspondence and reciprocity of feelings that can be generated with an adult.

Primordial motive systems appear in subcortical and limbic systems of the embryo before the cerebral cortex. These are presumed to continue to guide the growth of a child's brain after birth. We propose that an “intrinsic motive formation” is assembled prenatally and is ready at birth to share emotion with caregivers for regulation of the child's cortical development, on which cultural cognition and learning depend.

The intrinsic potentiality for “intersubjectivity” can be disorganized if the epigenetic program for the infant's brain fails. Indeed, many psychological disorders of childhood can be traced to faults in early stages of brain development when core motive systems form.

The term plasticity is often confined to changes due to learning. We believe, however, that the rapid lability of human behavior as different mental contents receive attention represents an important form of plasticity. Recent research in temperament and cognitive neuroscience provides an account of the development of a specific neural system involved in attentional self-regulation. In this paper, we concentrate on a network involved in orienting. We describe what is currently known about this network and its development during the first years of life. This network interacts with other attentional networks that come to control orienting to remembered events as well as those currently present. Orienting reflects processes that are both deeply biological and also open to cultural influences through learning. Attention is influenced by the current emotional state and is also important in achieving control over the emotional state. We present evidence on how learning influences eye position between 4 and 18 months of life and indicate influences of orienting on important aspects of infant behavior. Like any biological system, problems can arise in these mechanisms. We speculate on how individual differences in distress proneness and orienting may relate to the development of psychopathology.

This paper explores the development of cortical plasticity and cognitive representations in light of temperamental differences in basic motivational systems. Motivational systems related to reward/approach and punishment/avoidance begin to function early in life. By controlling the child's behavioral and emotional reactions, these systems provide exteroceptive and interoceptive information capable of stabilizing cortical synapses through use-dependent processes. By controlling attention, the motivational systems further contribute to synaptic stabilization through modulatory processes. As a result, children with strong reward/approach systems are likely to develop representations that emphasize potential rewards and frustrations and may become vulnerable to impulsive disorders. Children with strong punishment/avoidance systems may develop representations emphasizing punishment and relief, along with a vulnerability to anxiety disorders. These motivationally constructed representations differentiate in varied ways across domains involving the physical world, moral rules, and the self and, thus, contribute to the various forms of impulsive and anxious psychopathology.

Three models that can be used to investigate the effects of different environmental events on brain development and organization are explored. The insult model argues against brain plasticity, and the environmental model regards the brain as infinitely plastic. Our work is guided by the transactional model, which views brain development and organization as an interaction between (a) genetically coded programs for the formation and connectivity of brain structures and (b) environmental modifiers of these codes. Data are reported from our cognitive and socioemotional research studies that support the notion of plasticity during the first 2 years of life. From our work with normal developmental processes, we draw parallels to abnormal development and speculate how the transactional model can be used to explain abnormal brain organization and development.

In this paper we discuss the contribution of neural activity-dependent factors to shaping the brain in normal and pathologic development, and we discuss factors that determine the likelihood of recovery from the experience of abnormal neural activity during development.

As modern neuroscience seeks to understand the neural bases for mental illness, it is becoming increasingly important to define how and when complex neural circuits may be altered in individuals who carry the genetic vulnerability for psychopathology. One factor that could potentially play a contributory role in mental illness is the stress response. A variety of studies suggest that stress can alter the activity of several key cortical neurotransmitters, including glutamate, γ-aminobutyric acid, dopamine, and serotonin. Specifically, exposure to neurotoxic levels of adrenal steroid hormone, particularly if this occurs early in life, could potentially induce permanent changes of these transmitter systems in corticolimbic regions, such as the hippocampal formation and cingulate gyrus, that have a high density of glucocorticoid receptors. Overall, exposure to severe stress during the perinatal period could potentially induce alterations in the circuitry of the anterior cingulate cortex and hippocampal formation and interfere with the normal mechanisms underlying attention and learning.

A model of asymmetric contributions to the control of different subcomponents of approach- and withdrawal-related emotion and psychopathology is presented. Two major forms of positive affect are distinguished. An approach-related form arises prior to goal attainment, and another form follows goal attainment. The former is hypothesized to be associated with activation of the left prefrontal cortex. Individual differences in patterns of prefrontal activation are stable over time. Hypoactivation in this region is proposed to result in approach-related deficits and increase an individual's vulnerability to depression. Data in support of these proposals are presented. The issue of plasticity is then considered from several perspectives. Contextual factors are superimposed upon tonic individual differences and modulate the magnitude of asymmetry. Pharmacological challenges also alter patterns of frontal asymmetry. A diverse array of evidence was then reviewed that lends support to the notion that these patterns of asymmetry may be importantly influenced by early environmental factors that result in enduring changes in brain function and structure.

Dramatic changes take place in the neural physiology and emotional behavior of the human infant during the first 2 years of life. Evidence suggests that certain variations in the infant's early social environment, such as disturbances in mother-infant interaction that are associated with maternal depression, influence the development of biological systems related to the expression and regulation of emotion, particularly those systems involved in frontal lobe, autonomic, and adrenocortical functioning. In this essay, we provide an overview of the links between maternal depression and disruptions in early social and emotional development, and we highlight parallels between disturbances in biological systems found in depressed adults and those found in infants of mothers experiencing depression. We then discuss the possibility of sensitive periods for the enduring influences of maternal depression on the emotional development of these children and for increased risk for affective disorder. Finally, we point to directions for further research on the nature of the intergenerational transmission of emotional disturbance.

Electrophysiological kindling and behavioral sensitization to psychomotor stimulants and stress provide paradigms for understanding how repeated acute events can leave neurobiological residues in gene expression, accounting for the observed long-lasting alterations in behavioral responsivity. Kindling helps conceptualize how repeated electrical stimulation of the brain can progressively evoke increased behavioral and convulsive responsivity, leading to spontaneous seizures in the absence of exogenous stimulation following sufficient stimulations. As kindling unfolds, a complex spatiotemporal cascade of events occurs and includes the induction of immediate early genes (e.g., c-fos) and late effector genes (including peptides and growth factors) possibly associated with the observed changes in brain microstructure (e.g., synapse formation, axonal and dendritic sprouting, apoptosis). Behavioral sensitization to psychomotor stimulants and stress has also been shown to induce related but different cascades of effects on immediate early and late effector gene expression. These may be associated with the observed long-lasting alterations in behavioral responsivity based on prior experience. If these types of alterations are put into a developmental context, this would provide a paradigm for understanding how early life events could exert profound and behaviorally relevant biochemical and microstructural effects on the central nervous system of the developing organism. The conceptual overview offered by the sensitization and kindling models suggests that environmentally triggered neurobiological processes do not form a single or static residue but, instead, engage processes related to developmental neurobiology and learning and memory and whose substrate is constantly evolving over an organism's lifetime.