See also Glossary for abbreviations used in this article.
On the resilience of remote traumatic memories against exposure therapy-mediated attenuation
Article first published online: 16 JUL 2014
© 2014 The Authors
Volume 15, Issue 8, pages 853–861, August 2014
How to Cite
EMBO Reports (2014) 15: 853–861
- Issue published online: 1 AUG 2014
- Article first published online: 16 JUL 2014
- Manuscript Revised: 4 JUN 2014
- Manuscript Accepted: 4 JUN 2014
- Manuscript Received: 14 APR 2014
- US National Institutes of Health. Grant Number: NS078839
- histone acetylation;
- remote memories
How to attenuate traumatic memories has long been the focus of intensive research efforts, as traumatic memories are extremely persistent and heavily impinge on the quality of life. Despite the fact that traumatic memories are often not readily amenable to immediate intervention, surprisingly few studies have investigated treatment options for remote traumata in animal models. The few that have unanimously concluded that exposure therapy-based approaches, the most successful behavioral intervention for the attenuation of recent forms of traumata in humans, fail to effectively reduce remote fear memories. Here, we provide an overview of these animal studies with an emphasis on why remote traumatic memories might be refractory to behavioral interventions: A lack of neuroplasticity in brain areas relevant for learning and memory emerges as a common denominator of such resilience. We then outline the findings of a recent study in mice showing that by combining exposure therapy-like approaches with small molecule inhibitors of histone deacetylases (HDACis), even remote memories can be persistently attenuated. This pharmacological intervention reinstated neuroplasticity to levels comparable to those found upon successful attenuation of recent memories. Thus, HDACis—or any other agent capable of heightening neuroplasticity—in conjunction with exposure therapy-based treatments might constitute a promising approach to overcome remote traumata.