Impact Factor 3.138
2017 JCR, Clarivate Analytics 2018

The world's most-cited Neurosciences journals

Review ARTICLE Provisionally accepted The full-text will be published soon. Notify me

Front. Behav. Neurosci. | doi: 10.3389/fnbeh.2019.00113

Stress across generations: DNA methylation as a potential mechanism underlying intergenerational effects of stress in both posttraumatic stress disorder and pre-clinical predator stress rodent models.

  • 1Memorial University of Newfoundland, Canada
  • 2Université Pierre et Marie Curie, France

Although most humans will experience some type of traumatic event in their lifetime only a small set of individuals will go on to develop posttraumatic stress disorder (PTSD). Differences in sex, age, trauma type, and comorbidity, along with many other elements, contribute to the heterogenous manifestation of this disorder. Nonetheless, aberrant hypothalamus-pituitary-adrenal (HPA) axis activity, especially in terms of cortisol and glucocorticoid receptor (GR) alterations, has been postulated as a tenable factor in the etiology and pathophysiology of PTSD. Moreover, emerging data suggests that the harmful effects of traumatic stress to the HPA axis in PTSD can also propagate into future generations, making offspring more prone to psychopathologies. Predator stress models provide an ethical and ethologically relevant way to investigate tentative mechanisms that are thought to underlie this phenomenon. In this review, we discuss findings from human and laboratory predator stress studies that suggest changes to DNA methylation germane to GRs may underlie the generational effects of trauma transmission. Understanding mechanisms that promote stress-induced psychopathology will represent a major advance in the field, and may lead to novel treatments for such devastating, and often treatment-resistant trauma and stress-disorders.

Keywords: PTSD (post traumatic stress disorder), predator stress, DNA Methylation, Glucocorticoid receptor, FKBP5 DNA methylation

Received: 06 Dec 2018; Accepted: 07 May 2019.

Edited by:

Tamas Kozicz, Mayo Clinic, United States

Reviewed by:

Balazs Gaszner, University of Pécs, Hungary
Chadi Touma, University of Osnabrück, Germany
Dora Zelena, Institute of Experimental Medicine (MTA), Hungary  

Copyright: © 2019 Bhattacharya, Fontaine, MacCallum, Drover and Blundell. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: Dr. Jacqueline J. Blundell, Memorial University of Newfoundland, St. John's, NL A1C 5S7, Newfoundland and Labrador, Canada,