The plan is to describe the changes in neuronal mechanisms that are associated with two important transitions in brain development—the transition from prenatal to postnatal life and the transition from puberty to adulthood. Until birth, developmental processes are controlled mainly by biochemical signaling systems that read structural information from genes and regulate gene expression as a function of developmental progress. This process continues until puberty but gets progressively more under the control of electrical activity generated by the maturing nerve nets. Since sense organs become functional after birth, this electrical activity is modulated to a large extent by sensory signals, and hence experience assumes the role of an important shaping factor for the development of neuronal architectures. During this phase of development, experience leads to irreversible modifications of the genetically determined blueprint of neuronal connections. In this process, cognitive and motor functions are adapted to the actual requirements of the encountered environment, and neuronal resources become assigned to particular functions as a result of exercise. Around the time of puberty, the developmental processes proper such as the formation and breaking of synaptic connections come to an end, but experience continues to modulate the functions of the now crystallized anatomical substrate by modifying the strength of established synaptic connections. This process is the basis for adult learning. Particular emphasis is laid on the evidence that these adaptive processses are all supervised by central gating systems that permit changes only in response to activity patterns that are identified as concordant with genetically prespecified expectancies of the developing brain and that are identified as behaviorally relevant. Together with the well-defined rules that govern experience-dependent modifications of the neuronal architecture and of synaptic weights, this constrains the range of modifications that can be induced by early imprinting and subsequent learning. Also explored is the extent to which the knowledge about these constraining factors is relevant for educational programs intended to unfold latent capacities, to encourage the development of special skills, and to rescue functions that have either failed to develop or were lost as a consequence of disease.
KeywordsSchizophrenia Retina Coherence NMDA Cholin
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