Stress, epigenetic control of gene expression and memory formation

Exp Neurol. 2012 Jan;233(1):3-11. doi: 10.1016/j.expneurol.2011.03.022. Epub 2011 Apr 2.


Making memories of a stressful life event is essential for an organism's survival as it allows it to adapt and respond in a more appropriate manner should the situation occur again. However, it may be envisaged that extremely stressful events can lead to formation of traumatic memories that are detrimental to the organism and lead to psychiatric disorders such as post-traumatic stress disorder (PTSD). The neurotransmitter glutamate and the ERK MAPK signaling pathway play a principal role in learning and memory. Glucocorticoid hormones acting via the glucocorticoid receptor have been shown to strengthen the consolidation of memories of stressful events. The ERK MAPK signaling pathway and glucocorticoid receptor-mediated actions have recently been shown to drive epigenetic modifications and conformational changes in the chromatin, stimulating the expression of neuroplasticity-related genes involved in stress-related learning and memory processes. The main epigenetic regulatory mechanisms are histone modifications and DNA (de-)methylation. Recently, studies have demonstrated that these processes are acting together in concert to regulate gene expression required for memory consolidation. This review explores the role of stress in learning and memory paradigms and the participating signaling pathways and epigenetic mechanisms and the enzymes that control these modifications during the consolidation process of memory formation.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Epigenesis, Genetic*
  • Epigenomics
  • Gene Expression / genetics*
  • Glucocorticoids / metabolism
  • Histones / metabolism
  • Humans
  • Memory / physiology*
  • Signal Transduction / genetics
  • Stress, Psychological / genetics
  • Stress, Psychological / physiopathology*


  • Glucocorticoids
  • Histones