Abstract
There are numerous examples of enduring effects of early experience on gene transcription and neural function. We review the emerging evidence for epigenetics as a candidate mechanism for such effects. There is now evidence that intracellular signals activated by environmental events can directly modify the epigenetic state of the genome, including CpG methylation, histone modifications and microRNAs. We suggest that this process reflects an activity-dependent epigenetic plasticity at the level of the genome, comparable with that observed at the synapse. This epigenetic plasticity mediates neuronal differentiation and phenotypic plasticity, including that associated with learning and memory. Altered epigenetic states are also associated with the risk for and expression of mental disorders. In a broader context, these studies define a biological basis for the interplay between environmental signals and the genome in the regulation of individual differences in behavior, cognition and physiology, as well as the risk for psychopathology.
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