Experience effects on brain development: possible contributions to psychopathology

Abstract

Researchers and clinicians are increasingly recognizing that psychological and psychiatric disorders are often developmentally progressive, and that diagnosis often represents a point along that progression that is defined largely by our abilities to detect symptoms. As a result, strategies that guide our searches for the root causes and etiologies of these disorders are beginning to change. This review describes interactions between genetics and experience that influence the development of psychopathologies. Following a discussion of normal brain development that highlights how specific cellular processes may be targeted by genetic or environmental factors, we focus on four disorders whose origins range from genetic (fragile X syndrome) to environmental (fetal alcohol syndrome) or a mixture of both factors (depression and schizophrenia). C.H. Waddington's canalization model (slightly modified) is used as a tool to conceptualize the interactive influences of genetics and experience in the development of these psychopathologies. Although this model was originally proposed to describe the 'canalizing' role of genetics in promoting normative development, it serves here to help visualize, for example, the effects of adverse (stressful) experience in the kindling model of depression, and the multiple etiologies that may underlie the development of schizophrenia. Waddington's model is also useful in understanding the canalizing influence of experience-based therapeutic approaches, which also likely bring about 'organic' changes in the brain. Finally, in light of increased evidence for the role of experience in the development and treatment of psychopathologies, we suggest that future strategies for identifying the underlying causes of these disorders be based less on the mechanisms of action of effective pharmacological treatments, and more on increased knowledge of the brain's cellular mechanisms of plastic change.

Reduced Dendritic Spine Density in Auditory Cortex of Subjects with Schizophrenia

“…It has been proposed that reduced excitatory connectivity in subjects with schizophrenia may result either from failure to initially elaborate sufficient numbers of such synapses, excess elimination of these synapses due to experience-dependent plasticity (Grossman et al, 2003), or both (Feinberg, 1982;Keshavan et al, 1994;Mirnics et al, 2001). Our findings cannot differentiate between these three possibilities.…”

The Role of Nutrition in Children's Neurocognitive Development, From Pregnancy Through Childhood

“…Brain development is a temporally extended and complex process, with different parts and functions of the brain developing at different times (Grossman et al, 2003). By 5 weeks after conception in humans, the anterior-posterior and dorsal-ventral axes of the neural tube have already developed (Levitt, 2003).…”

The systems approach in developmental psychology: fundamental concepts and principles

“…Among other examples, the author refers to the role of visual experience in activating the gene that codes for tubilin, an integral protein in the axons and dendrites that support the functional connections of the visual system. In more recent studies, Greenough and co-workers reviewed experience effects on brain development (see for example Grossman et al, 2003;Kramer et al, 2004). Gottlieb (1991Gottlieb ( , 1997 distinguished the biological levels of neural activity and genetic activity, a third level of behavior and the last one formed by physical, social and cultural aspects of environment.…”

“…In a recent study, Grossman et al (2003) integrated this dual genetic and environmental regulating action, in an attempt to explain the pathological deviations of normal psychological development. To do so, they took Waddington's metaphor of canalization and included non-genetic canalizing experiences that were absent in the original proposal.…”