Dissection of the cellular and molecular mechanisms governing well-established critical periods represents a powerful tool to identify new potential therapeutic targets to restore normal plasticity and function in affected neuronal circuits.
The developing brain is remarkably malleable, capable of restructuring synaptic connections in response to changing experiences.
Critical periods close after a cascade of structural consolidation of neuronal circuits and their connectivity, preventing future plasticity as the brain reaches adulthood.
These sensitive periods of elevated plasticity are times of opportunity but also of great vulnerability for the developing brain.
The underlying cause is still largely unknown and there is no fully effective treatment or cure.
We propose that alteration of the expression and/or timing of critical period circuit refinement in primary sensory brain areas may significantly contribute to autistic phenotypes, including cognitive and behavioral impairments.
Cortical circuits in the brain are refined by experience during critical periods early in postnatal life.
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The basic layout of the brain is first established by genetic programs and intrinsic activity and is then actively refined by the surrounding environment in which the individual is immersed .
This experience-dependent sculpting of neuronal circuits occurs during distinct time windows called critical periods .