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Author Notes:

G. N. Neigh, Department of Psychiatry and Behavioral Sciences, Emory University, 615 Michael Street, Suite 600, Atlanta, GA 30322, United States. Tel: +1-404-727-9022; fax: +1-404-727-2648., gretchen.neigh@emory.edu, gmccand@emory.edu

Subjects:

Keywords:

  • Science & Technology
  • Life Sciences & Biomedicine
  • Neurosciences
  • Neurosciences & Neurology
  • stress
  • trauma
  • PTSD
  • adolescent
  • preclinical
  • animal model
  • CORTICOTROPIN-RELEASING-FACTOR
  • LONG-TERM CONSEQUENCES
  • ANIMAL-MODEL
  • RISK-FACTORS
  • CHILDHOOD MALTREATMENT
  • FKBP5 POLYMORPHISMS
  • PROLONGED EXPOSURE
  • SOCIAL INFLUENCES
  • RAT HYPOTHALAMUS
  • PTSD COMORBIDITY

Translational Reciprocity:Bridging the gap between preclinical studies and clinical treatment of stress effects on the adolescent brain

Tools:

Journal Title:

Neuroscience

Volume:

Volume 249

Publisher:

, Pages 139-153

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The genetic, biological, and environmental backgrounds of an organism fundamentally influence the balance between risk and resilience to stress. Sex, age, and environment transact with responses to trauma in ways that can mitigate or exacerbate the likelihood that post-traumatic stress disorder will develop. Translational approaches to modeling affective disorders in animals will ultimately provide novel treatments and a better understanding of the neurobiological underpinnings behind these debilitating disorders. The extant literature on trauma/stress has focused predominately on limbic and cortical structures that innervate the hypothalamic-pituitary-adrenal axis and influence glucocorticoid-mediated negative feedback. It is through these neuroendocrine pathways that a self-perpetuating fear memory can propagate the long-term effects of early life trauma. Recent work incorporating translational approaches has provided novel pathways that can be influenced by early life stress, such as the glucocorticoid receptor chaperones, including FKBP51. Animal models of stress have differing effects on behavior and endocrine pathways; however, complete models replicating clinical characteristics of risk and resilience have not been rigorously studied. This review discusses a four-factor model that considers the importance of studying both risk and resilience in understanding the developmental response to trauma/stress. Consideration of the multifactorial nature of clinical populations in the design of preclinical models and the application of preclinical findings to clinical treatment approaches comprise the core of translational reciprocity, which is discussed in the context of the four-factor model.

Copyright information:

© 2012 IBRO. Published by Elsevier Ltd. All rights reserved.

This is an Open Access work distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License (http://creativecommons.org/licenses/by-nc-nd/4.0/).

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