Environmental Regulation Of The Neural Epigenome

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.

KEYWORDS::

• DNA methylation
• early experience
• histone modifications
• learning and memory
• psychopathology

Financial & competing interests disclosure

Research support for Michael J Meaney is provided by the National Institutes of Health, the Canadian Institutes for Health Research, the Natural Sciences and Engineering Research Council of Canada, and the Human Frontiers Science Program. Judy Sng and Michael J Meaney are supported by A*STAR funding for the Integrative Neuroscience Program of the Singapore Institute for Clinical Sciences. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

Research support for Michael J Meaney is provided by the National Institutes of Health, the Canadian Institutes for Health Research, the Natural Sciences and Engineering Research Council of Canada, and the Human Frontiers Science Program. Judy Sng and Michael J Meaney are supported by A*STAR funding for the Integrative Neuroscience Program of the Singapore Institute for Clinical Sciences. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript.