The DOI matches its Crossref record; 117 of the 117 references it cites were found in a registry or an index.
The role of the genome in experience-dependent plasticity: Extending the analogy of the genomic action potential
Abstract
Our past experiences shape our current and future behavior. These experiences must leave some enduring imprint on our brains, altering neural circuits that mediate behavior and contributing to our individual differences. As a framework for understanding how experiences might produce lasting changes in neural circuits, Clayton [D. F. Clayton, Neurobiol. Learn. Mem. 74, 185–216 (2000)] introduced the concept of the genomic action potential (gAP)—a structured genomic response in the brain to acute experience. Similar to the familiar electrophysiological action potential (eAP), the gAP also provides a means for integrating afferent patterns of activity but on a slower timescale and with longer-lasting effects. We revisit this concept in light of contemporary work on experience-dependent modification of neural circuits. We review the “Immediate Early Gene” (IEG) response, the starting point for understanding the gAP. We discuss evidence for its involvement in the encoding of experience to long-term memory across time and biological levels of organization ranging from individual cells to cell ensembles and whole organisms. We explore distinctions between memory encoding and homeostatic functions and consider the potential for perpetuation of the imprint of experience through epigenetic mechanisms. We describe a specific example of a gAP in humans linked to individual differences in the response to stress. Finally, we identify key objectives and new tools for continuing research in this area.
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“For instance, early adverse experiences have been shown to prime the genome, via DNA methylation at specific loci related to stress-response pathways, so that the individual responds differently to future stressful events (78–80).”
From Behavior-related gene regulatory networks: A new level of organization in the brain (2020) · cites this paper as [79]
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HDAC2 negatively regulates memory formation and synaptic plasticity
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Allele-specific FKBP5 DNA demethylation mediates gene–childhood trauma interactions
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Self-citationBDNF: A Key Factor with Multipotent Impact on Brain Signaling and Synaptic Plasticity
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Research works printed but not linked: 2
- 10.1016/j.cell.2017.12.024 · DOI · Paper page
- D. O. Hebb The Organization of Behaviour: A Neuropsychological Theory (John Wiley and Sons New York NY 1949).
Cited by
Behavior-related gene regulatory networks: A new level of organization in the brain
Sinha, S., Jones, B. M., Traniello, I. M., Bukhari, S. A., Halfon, M. S., Hofmann, H. A., Huang, S., Katz, P. S., Keagy, J., Lynch, V. J., et al. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1921625117 · Cited by 85
Multigenerational epigenetic inheritance: One step forward, two generations back
Tuscher, J. J., & Day, J. J. (2019) · Neurobiology of Disease · doi:10.1016/j.nbd.2019.104591 · Cited by 63
Metadata
- Authors
- Clayton, D. F., Anreiter, I., Aristizabal, M., Frankland, P. W., Binder, E. B., & Citri, A.
- Affiliations
- Program in Child and Brain Development, Canadian Institute for Advanced Research, Toronto, ON M5G 1M1, Canada;
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 2019-05-24
- Volume
- 117
- Issue
- 38
- Pages
- 23252-23260
- ISSN
- 0027-8424
- 1091-6490
- Cited by
- 56
- References
- 117
- Language
- en
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