Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans.

Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

This review critically summarizes the neuropathology and genetics of schizophrenia, the relationship between them, and speculates on their functional convergence. The morphological correlates of schizophrenia are subtle, and range from a slight reduction in brain size to localized alterations in the morphology and molecular composition of specific neuronal, synaptic, and glial populations in the hippocampus, dorsolateral prefrontal cortex, and dorsal thalamus. These findings have fostered the view of schizophrenia as a disorder of connectivity and of the synapse. Although attractive, such concepts are vague, and differentiating primary events from epiphenomena has been difficult. A way forward is provided by the recent identification of several putative susceptibility genes (including neuregulin, dysbindin, COMT, DISC1, RGS4, GRM3, and G72). We discuss the evidence for these and other genes, along with what is known of their expression profiles and biological roles in brain and how these may be altered in schizophrenia. The evidence for several of the genes is now strong. However, for none, with the likely exception of COMT, has a causative allele or the mechanism by which it predisposes to schizophrenia been identified. Nevertheless, we speculate that the genes may all converge functionally upon schizophrenia risk via an influence upon synaptic plasticity and the development and stabilization of cortical microcircuitry. NMDA receptor-mediated glutamate transmission may be especially implicated, though there are also direct and indirect links to dopamine and GABA signalling. Hence, there is a correspondence between the putative roles of the genes at the molecular and synaptic levels and the existing understanding of the disorder at the neural systems level. Characterization of a core molecular pathway and a 'genetic cytoarchitecture' would be a profound advance in understanding schizophrenia, and may have equally significant therapeutic implications.

Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergence.

BDNF function in adult synaptic plasticity: the synaptic consolidation hypothesis.

Glutamate receptor function in learning and memory

How do minds emerge from developing brains? According to "neural constructivism," the representational features of cortex are built from the dynamic interaction between neural growth mechanisms and environmentally derived neural activity. Contrary to popular selectionist models that emphasize regressive mechanisms, the neurobiological evidence suggests that this growth is a progressive increase in the representational properties of cortex. The interaction between the environment and neural growth results in a flexible type of learning: "constructive learning" minimizes the need for prespecification in accordance with recent neurobiological evidence that the developing cerebral cortex is largely free of domain-specific structure. Instead, the representational properties of cortex are built by the nature of the problem domain confronting it. This uniquely powerful and general learning strategy undermines the central assumption of classical learnability theory, that the learning properties of a system can be deduced from a fixed computational architecture. Neural constructivism suggests that the evolutionary emergence of neocortex in mammals is a progression toward more flexible representational structures, in contrast to the popular view of cortical evolution as an increase in innate, specialized circuits. Human cortical postnatal development is also more extensive and protracted than generally supposed, suggesting that cortex has evolved so as to maximize the capacity of environmental structure to shape its structure and function through constructive learning.

/pdf/the-neural-basis-of-cognitive-development-a-constructivist-meee8ey9rg.pdf

The neural basis of cognitive development: a constructivist manifesto.

Neocortical synaptogenesis, aging, and behavior: Lifespan development in the motor-sensory system of the rat

The role of synaptic morphology in neural plasticity: structural interactions underlying synaptic power

Neonatal lead exposure alters the dendritic development of hippocampal dentate granule cells

Neurofibrillary degeneration, dendritic dying back, and learning-memory deficits after aluminum administration: Implications for brain aging

Neurobiology of Down's syndrome

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