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Chapter 24 Summary

An individual animal’s history of interaction with its environment— its “experience”—helps shape its neural circuitry and thus determines subsequent behavior. Experience during specific times in early life, referred to as critical periods, helps shape behaviors as diverse as maternal bonding and the acquisition of language. Correlated patterns of activity are thought mediate critical periods by stabilizing concurrently active synaptic connections and weakening or eliminating connections whose activity is divergent. The cellular and molecular mechanisms implicated in critical periods rely on the activity of several neurotransmitters, receptors, and intracellular signaling cascades that modify gene expression in response to changes in synaptic activity in a target cell. Genes for neurotrophins such as BDNF, extracellular matrix components, and neurotransmitter receptors are all targets for altered expression in response to synaptic activity during critical periods. The most accessible and thoroughly studied example of a critical period is that responsible for the establishment of normal vision. These studies show that experience is translated into patterns of neuronal activity that influence the function and connectivity of neurons in the visual cortex. When normal patterns of activity are disturbed during the critical period in early life (experimentally in animals or by pathology in humans), connectivity in the visual cortex is altered, as is visual function. If not reversed before the end of the critical period, these structural and functional alterations of brain circuitry are difficult or impossible to change. Observations of the addition and elimination of synapses throughout the cerebral cortex in animals, and parallel analysis of the increase and decrease of cortical gray matter volumes in children and adolescents, indicate that a full range of human behaviors— including those compromised in conditions such as autism, schizophrenia, and ADHD—may be shaped by activity and experience-dependent addition and subsequent elimination of synaptic connections during critical periods that begin at birth and end in early adulthood.

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