Using the Single Prolonged Stress Model to Examine the Pathophysiology of PTSD

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dc.contributor.authorSouza, Rimenez R.en_US
dc.contributor.authorNoble, Lindsey J.en_US
dc.contributor.authorMcIntyre, Christa K.en_US
dc.contributor.utdAuthorSouza, Rimenez R.en_US
dc.contributor.utdAuthorNoble, Lindsey J.en_US
dc.contributor.utdAuthorMcIntyre, Christa K.en_US
dc.date.accessioned2018-09-24T15:30:19Z
dc.date.available2018-09-24T15:30:19Z
dc.date.created2017-09-11
dc.description.abstractThe endurance of memories of emotionally arousing events serves the adaptive role of minimizing future exposure to danger and reinforcing rewarding behaviors. However, following a traumatic event, a subset of individuals suffers from persistent pathological symptoms such as those seen in posttraumatic stress disorder (PTSD). Despite the availability of pharmacological treatments and evidence-based cognitive behavioral therapy, a considerable number of PTSD patients do not respond to the treatment, or show partial remission and relapse of the symptoms. In controlled laboratory studies, PTSD patients show deficient ability to extinguish conditioned fear. Failure to extinguish learned fear could be responsible for the persistence of PTSD symptoms such as elevated anxiety, arousal, and avoidance. It may also explain the high non-response and dropout rates seen during treatment. Animal models are useful for understanding the pathophysiology of the disorder and the development of new treatments. This review examines studies in a rodent model of PTSD with the goal of identifying behavioral and physiological factors that predispose individuals to PTSD symptoms. Single prolonged stress (SPS) is a frequently used rat model of PTSD that involves exposure to several successive stressors. SPS rats show PTSD-like symptoms, including impaired extinction of conditioned fear. Since its development by the Liberzon lab in 1997, the SPS model has been referred to by more than 200 published papers. Here we consider the findings of these studies and unresolved questions that may be investigated using the model.en_US
dc.description.departmentSchool of Behavioral and Brain Sciencesen_US
dc.description.departmentTexas Biomedical Device Centeren_US
dc.description.sponsorshipGrant/Contract No. DARPA-BAA-14-38 and DARPA-BAA-15-06; NIMH No. MH105014en_US
dc.identifier.bibliographicCitationSouza, Rimenez R., Lindsey J. Noble, and Christa K. McIntyre. 2017. "Using the single prolonged stress model to examine the pathophysiology of PTSD." 8, doi:10.3389/fphar.2017.00615en_US
dc.identifier.issn1663-9812en_US
dc.identifier.urihttp://hdl.handle.net/10735.1/6111
dc.identifier.volume8en_US
dc.publisherFrontiers Media SAen_US
dc.relation.urihttp://dx.doi.org/10.3389/fphar.2017.00615en_US
dc.rightsCC BY 4.0 (Attribution)en_US
dc.rights©2017 The Authorsen_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/en_US
dc.source.journalFrontiers in Pharmacologyen_US
dc.subjectModels, Animalen_US
dc.subjectFearen_US
dc.subjectGlucocorticoidsen_US
dc.subjectStress Disorders, Post-Traumaticen_US
dc.subjectStress, Psychologicalen_US
dc.subjectExtinction, Psychologicalen_US
dc.subjectStress, Physiologicalen_US
dc.titleUsing the Single Prolonged Stress Model to Examine the Pathophysiology of PTSDen_US
dc.typeTexten_US
dc.type.genrearticleen_US

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