In a recent article, Cowan, Harter, and Kandel (2000) concluded that much of the success and excitement engendered by modern neuroscience can be attributed to the incorporation of several previously independent disciplines into one intellectual framework. During the 1950s and 1960s, neuroanatomy, neurochemistry, neuropharmacology, and neurophysiology, disciplines that had largely functioned in a separate and distinct fashion, gradually merged into a unified field of neuroscience. The penultimate step in the coalescence of neuroscience occurred in the early 1980s, when neuroscience integrated with molecular biology and molecular genetics. The confluence of these fields enabled scientists to understand the genetic basis of neurological diseases for the first time without requiring foreknowledge of the underlying biochemical abnormalities. The final phase of the merger of neuroscience into a single discipline took place in the mid-1980s, when cognitive psychology joined with neuroscience, leading to the formation of cognitive neuroscience.

An understanding of developmental phenomena demands a relational or coactive concept of causality, as opposed to a conceptualization that assumes that singular causes can act in isolation. In this article we present a developmental psychobiological systems view of relational (bidirectional, coactional) causality, in which it is proposed that developmental outcomes are a consequence of at least two specific components of coaction from the same or different levels of a developmental system. The levels are genetic, neural, behavioral, and environmental; the latter level includes the cultural, social, and physical aspects of an organism's environment. We show the applicability of this view to the understanding of the development of normal and abnormal behavioral and psychological phenotypes through illustrations from the existing animal and human literature. Finally, we discuss future possibilities and potential stumbling blocks in the implementation of a more fully realized bidirectional, coactional perspective in developmental psychopathological research.

Most of the major psychiatric disorders have been analyzed at each of several different levels. For example, at the broadest level, epidemiological studies have served to establish the incidence of disorders like schizophrenia and major depression in a number of different populations. Family and twin studies have been important in determining the heritability of certain mental illnesses, and chromosomal and linkage analyses have identified a number of discrete loci that appear to be implicated in disease susceptibility or, even directly, in the pathogenesis of some disorders. In a few cases, specific genes have been found to be mutated or polymorphic and proteins they encode are currently being analyzed. This article reviews how these different levels contribute to our understanding of a number of psychiatric disorders, including drug addiction, which has been the focus of much of our own work.

This paper tries to make three points. First, current constructs in personality and psychopathology are based on the restrictive evidence contained in self-reports. As a result, heterogeneous categories of individuals are assigned to the same category. Second, it is suggested that when different sources of evidence are included, theoretically distinct groups will be detected within the prior heterogeneous category. Third, the authors argue that physiological information has the potential to parse individuals with similar phenotypes on self-report data into distinct groups that reveal the temperamental origins of their phenotype.

Self-regulatory processes are believed to be critical to early personality and behavioral adjustment. Such processes can be observed on multiple levels, including the physiological, attentional, emotional, cognitive, and interpersonal domains of functioning. Data from several longitudinal studies suggest links between early temperamental tendencies such as behavioral inhibition and frustration tolerance, and regulatory developments at the levels of physiological, attentional, and emotional regulation. Deficits in these particular levels of self-regulation may underlie childhood social withdrawal and aggression. Significant gaps remain in our knowledge of the pathways to disordered behavior and the role that self-regulation plays in such pathways. Suggestions are made for the ways in which future longitudinal studies might address these gaps.

The study of brain development and that of behavioral development have historically proceeded independently of one another. This is an unfortunate set of circumstances, given that the disciplines concerned with development—for example, developmental psychology, pediatrics, psychiatry, clinical psychology, and the neurosciences—have much to learn from each other. Drawing on recent advances in the developmental brain and behavioral sciences, we illustrate the transdisciplinary approach our group has adopted in the service of uniting the research on brain and behavior in the context of development. We specifically report on our nonhuman primate and human studies that collectively illustrate our “genes to behavior” approach to the study of development. Our goal in summarizing our research in this fashion is to promote discussion about promising templates for how research on brain, behavior, and development might proceed into the 21st century.

To date, research involving functional neuroimaging of typical and atypical development has depended on several assumptions about the postnatal maturation of the brain. We consider evidence from multiple levels of analysis that brings into question these underlying assumptions and advance an alternative view. This alternative view, based on an “interactive specialization” approach to postnatal brain development, indicates that there is a need to: obtain data from early in development; focus more on differences in interregional interactions rather than searching for localized, discrete lesions; examine the temporal dynamics of neural processing; and move away from deficits to image tasks in which atypical participants perform as well as typically developing participants.

The hypothesis that brain stem injury plays a role in the autism spectrum disorders was suggested by evidence that exposure to thalidomide during the earliest stages of brain development increases the risk of autism spectrum disorders. The implications for the embryological origin of autism first led to studies of neuroanatomy in a human case and an animal model and then to examinations of minor craniofacial features in autism. But the general hypothesis had much broader implications. It has now generated studies of the behavioral and neurological symptoms of human patients, of human molecular genetics and population genetics, and of animal behavioral teratology and molecular pharmacology. The collection of this range of data was made possible by adding experts from many fields to the research team. They worked both independently and collaboratively to try to unravel the etiology of autism.

Developmental language learning impairments (LLI) are one of the most prevalent of all developmental disabilities, can occur in children for a wide variety of reasons, and have been shown to co-occur frequently with other developmental social, emotional and behavioral disorders, as well as with academic achievement problems. Research pertaining to developmental LLI of unknown origin, with an emphasis on the continuum between oral and written language impairment, is the focus of this review. Given the complexity of language learning, research has focused on multiple levels of analysis, including linguistic, neuropsychological, genetic, neurobiological, and remediation studies. To date, the vast majority of data on LLI derive from studies focused on a single level of analysis. Although attempts have been made to integrate data across studies and multiple levels of analysis, this has proven to be problematic, given the heterogeneity of the subject populations used to study LLI, as well as the differences in ages, degree of impairment, and types of impairment included in each study. Given that LLI is a complex developmental disability, it is suggested that future research would benefit from taking a multiple levels of analysis approach with the same individuals, incorporating mathematical models designed to analyze dynamically changing complex systems, and studying individual differences in language learning, prospectively and longitudinally, throughout the most dynamic stages of the process.

Achieving progress in understanding the cause, nature, and treatment of autism requires an integration of concepts, approaches, and empirical findings from genetic, cognitive neuroscience, animal, and clinical studies. The need for such integration has been a fundamental tenet of the discipline of developmental psychopathology from its inception. It is likely that the discovery of autism susceptibility genes will depend on the development of dimensional measures of broader phenotype autism traits. It is argued that knowledge of the cognitive neuroscience of social and language behavior will provide a useful framework for defining such measures. In this article, the current state of knowledge of the cognitive neuroscience of social and language impairments in autism is reviewed. Following from this, six candidate broader phenotype autism traits are proposed: (a) face processing, including structural encoding of facial features and face movements, such as eye gaze; (b) social affiliation or sensitivity to social reward, pertaining to the social motivational impairments found in autism; (c) motor imitation ability, particularly imitation of body actions; (d) memory, specifically those aspects of memory mediated by the medial temporal lobe–prefrontal circuits; (e) executive function, especially planning and flexibility; and (f) Language ability, particularly those aspects of language that overlap with specific language impairment, namely, phonological processing.

Autism is a neurobiological disorder that is diagnosed through careful behavioral assessment in early childhood. In this paper, we review recent studies that have attempted to reveal the underlying causes of autism using a variety of techniques. Particular emphasis is placed on techniques that have been used by a number of different laboratories, including structural magnetic resonance imaging and postmortem studies of neuroanatomy. Neurobiological and neuropsychological data from individuals across a wide age range are examined from a neurodevelopmental perspective. We discuss how these recent advances have led us to develop a growth dysregulation hypothesis of autism. Finally, we discuss how this hypothesis may lead to new innovations in autism research.

In the authors' experience interactions between clinical and laboratory research have been greatly mutually facilitatory in the understanding and development of new treatments for the major mental illnesses. Examples in the literature are also highlighted to show how cross-disciplinary studies are important in understanding the subtle interactions of genetic and environmental mechanisms in psychiatric illness. Yet, the results of some current science policies encouraging project focus and superspecialization can lead to the separation of clinical and basic investigators, which threatens the integration of psychological complexity into the neurobiology of psychiatry at both a molecular and behavioral level. This paper endorses renewed effort toward the multidisciplinary team approach under the leadership of a physician–scientist in order to better integrate many fields of study critical to ameliorating the effects of psychiatric illness.

Etiological research spanning domains of inquiry as diverse as social psychology and molecular genetics has identified a number of potential factors that likely contribute to the development and clinical manifestation of schizophrenia. In this article, we first highlight the challenges inherent in developing cogent etiological models that represent both the diversity of suspected causal influences and their mechanisms of action. Then, using our own research program as a heuristic context, we present a general analytical framework for identifying and integrating multiple types of etiologic factors across different levels of analysis in the prediction of schizophrenia. In recognition of the myriad complexities of multifactorial causation, we argue that a multilevel causal perspective is required for the development and advancement of a fully nuanced theory of schizophrenia etiology and pathophysiology.