Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 May 15:9:196.
doi: 10.3389/fpsyt.2018.00196. eCollection 2018.

Single-Prolonged Stress: A Review of Two Decades of Progress in a Rodent Model of Post-traumatic Stress Disorder

Affiliations
Review

Single-Prolonged Stress: A Review of Two Decades of Progress in a Rodent Model of Post-traumatic Stress Disorder

Michael J Lisieski et al. Front Psychiatry. .

Abstract

Post-traumatic stress disorder (PTSD) is a common, costly, and often debilitating psychiatric condition. However, the biological mechanisms underlying this disease are still largely unknown or poorly understood. Considerable evidence indicates that PTSD results from dysfunction in highly-conserved brain systems involved in stress, anxiety, fear, and reward. Pre-clinical models of traumatic stress exposure are critical in defining the neurobiological mechanisms of PTSD, which will ultimately aid in the development of new treatments for PTSD. Single prolonged stress (SPS) is a pre-clinical model that displays behavioral, molecular, and physiological alterations that recapitulate many of the same alterations observed in PTSD, illustrating its validity and giving it utility as a model for investigating post-traumatic adaptations and pre-trauma risk and protective factors. In this manuscript, we review the present state of research using the SPS model, with the goals of (1) describing the utility of the SPS model as a tool for investigating post-trauma adaptations, (2) relating findings using the SPS model to findings in patients with PTSD, and (3) indicating research gaps and strategies to address them in order to improve our understanding of the pathophysiology of PTSD.

Keywords: HPA axis; PTSD; amygdala; anxiety; hippocampus; pre-clinical models; prefrontal cortex; single prolonged stress.

PubMed Disclaimer

Similar articles

Cited by

References

    1. APA Diagnostic and Statistical Manual of Mental Disorders. DSM 5. Arlington: American Psychiatric Association; (2013).
    1. Wang PS, Lane M, Olfson M, Pincus HA, Wells KB, Kessler RC. Twelve-month use of mental health services in the United States: results from the National Comorbidity Survey Replication. Arch Gen Psychiatry (2005) 62:629–40. 10.1001/archpsyc.62.6.629 - DOI - PubMed
    1. Watts BV, Schnurr PP, Mayo L, Young-Xu Y, Weeks WB, Friedman MJ. Meta-analysis of the efficacy of treatments for posttraumatic stress disorder. J Clin Psychiatry (2013) 74:541–50. 10.4088/JCP.12r08225 - DOI - PubMed
    1. Foa EB, Zinbarg R, Rothbaum BO. Uncontrollability and unpredictability in post-traumatic stress disorder: an animal model. Psychol Bull. (1992) 112:218. 10.1037/0033-2909.112.2.218 - DOI - PubMed
    1. Johnson LR, McGuire J, Lazarus R, Palmer AA. Pavlovian fear memory circuits and phenotype models of PTSD. Neuropharmacology (2012) 62:638–46. 10.1016/j.neuropharm.2011.07.004 - DOI - PubMed

LinkOut - more resources