3
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Cognitive Flexibility Training Improves Extinction Retention Memory and Enhances Cortical Dopamine With and Without Traumatic Stress Exposure

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Stress exposure can cause lasting changes in cognition, but certain individual traits, such as cognitive flexibility, have been shown to reduce the degree, duration, or severity of cognitive changes following stress. Both stress and cognitive flexibility training affect decision making by modulating monoamine signaling. Here, we test the role cognitive flexibility training, and high vs. low cognitive flexibility at the individual level, in attenuating stress-induced changes in memory and monoamine levels using the single prolonged stress (SPS) rodent model of traumatic stress in male Sprague-Dawley rats. Exposure to SPS can heighten fear responses to conditioned cues (i.e., freezing) after a fear association has been extinguished, referred to as a deficit in extinction retention. This deficit is thought to reflect an impairment in context processing that is characteristic of posttraumatic stress disorder (PTSD). During a cognitive flexibility training we assessed individual variability in cognitive skills and conditioned rats to discriminately use cues in their environment. We found that cognitive flexibility training, alone or followed by SPS exposure, accelerated extinction learning and decreased fear responses over time during extinction retention testing, compared with rats not given cognitive flexibility training. These findings suggest that cognitive flexibility training may improve context processing in individuals with and without traumatic stress exposure. Individual performance during the reversal phase of the cognitive flexibility training predicted subsequent context processing; individuals with high reversal performance exhibited a faster decrease in freezing responses during extinction retention testing. Thus, high reversal performance predicted enhanced retention of extinction learning over time and suggests that cognitive flexibility training may be a strategy to promote context processing. In a brain region vital for maintaining cognitive flexibility and fear suppression, the prelimbic cortex (PLC), cognitive flexibility training also lastingly enhanced dopamine (DA) and norepinephrine (NE) levels, in animals with and without traumatic stress exposure. In contrast, cognitive flexibility training prior to traumatic stress exposure decreased levels of DA and its metabolites in the striatum, a region mediating reflexive decision making. Overall, our results suggest that cognitive flexibility training can provide lasting benefits by enhancing extinction retention, a hallmark cognitive effect of trauma, and prelimbic DA, which can maintain flexibility across changing contexts.

          Related collections

          Most cited references92

          • Record: found
          • Abstract: found
          • Article: not found

          The Nature and Organization of Individual Differences in Executive Functions: Four General Conclusions.

          Executive functions (EFs)-a set of general-purpose control processes that regulate one's thoughts and behaviors-have become a popular research topic lately and have been studied in many subdisciplines of psychological science. This article summarizes the EF research that our group has conducted to understand the nature of individual differences in EFs and their cognitive and biological underpinnings. In the context of a new theoretical framework that we have been developing (the unity/diversity framework), we describe four general conclusions that have emerged from our research. Specifically, we argue that individual differences in EFs, as measured with simple laboratory tasks, (1) show both unity and diversity (different EFs are correlated yet separable); (2) reflect substantial genetic contributions; (3) are related to various clinically and societally important phenomena; and (4) show some developmental stability.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Neurobiological basis of failure to recall extinction memory in posttraumatic stress disorder.

            A clinical characteristic of posttraumatic stress disorder (PTSD) is persistently elevated fear responses to stimuli associated with the traumatic event. The objective herein is to determine whether extinction of fear responses is impaired in PTSD and whether such impairment is related to dysfunctional activation of brain regions known to be involved in fear extinction, viz., amygdala, hippocampus, ventromedial prefrontal cortex (vmPFC), and dorsal anterior cingulate cortex (dACC). Sixteen individuals diagnosed with PTSD and 15 trauma-exposed non-PTSD control subjects underwent a 2-day fear conditioning and extinction protocol in a 3-T functional magnetic resonance imaging scanner. Conditioning and extinction training were conducted on day 1. Extinction recall (or extinction memory) test was conducted on day 2 (extinguished conditioned stimuli presented in the absence of shock). Skin conductance response (SCR) was scored throughout the experiment as an index of the conditioned response. The SCR data revealed no significant differences between groups during acquisition and extinction of conditioned fear on day 1. On day 2, however, PTSD subjects showed impaired recall of extinction memory. Analysis of functional magnetic resonance imaging data showed greater amygdala activation in the PTSD group during day 1 extinction learning. During extinction recall, lesser activation in hippocampus and vmPFC and greater activation in dACC were observed in the PTSD group. The magnitude of extinction memory across all subjects was correlated with activation of hippocampus and vmPFC during extinction recall testing. These findings support the hypothesis that fear extinction is impaired in PTSD. They further suggest that dysfunctional activation in brain structures that mediate fear extinction learning, and especially its recall, underlie this impairment.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Neurocircuitry models of posttraumatic stress disorder and extinction: human neuroimaging research--past, present, and future.

              The prevailing neurocircuitry models of anxiety disorders have been amygdalocentric in form. The bases for such models have progressed from theoretical considerations, extrapolated from research in animals, to in vivo human imaging data. For example, one current model of posttraumatic stress disorder (PTSD) has been highly influenced by knowledge from rodent fear conditioning research. Given the phenomenological parallels between fear conditioning and the pathogenesis of PTSD, we have proposed that PTSD is characterized by exaggerated amygdala responses (subserving exaggerated acquisition of fear associations and expression of fear responses) and deficient frontal cortical function (mediating deficits in extinction and the capacity to suppress attention/response to trauma-related stimuli), as well as deficient hippocampal function (mediating deficits in appreciation of safe contexts and explicit learning/memory). Neuroimaging studies have yielded convergent findings in support of this model. However, to date, neuroimaging investigations of PTSD have not principally employed conditioning and extinction paradigms per se. The recent development of such imaging probes now sets the stage for directly testing hypotheses regarding the neural substrates of fear conditioning and extinction abnormalities in PTSD.
                Bookmark

                Author and article information

                Contributors
                Journal
                Front Behav Neurosci
                Front Behav Neurosci
                Front. Behav. Neurosci.
                Frontiers in Behavioral Neuroscience
                Frontiers Media S.A.
                1662-5153
                01 March 2019
                2019
                : 13
                : 24
                Affiliations
                [1] 1Department of Psychiatry and Behavioral Neurosciences, Wayne State University School of Medicine , Detroit, MI, United States
                [2] 2Research Service, John D. Dingell VA Medical Center , Detroit, MI, United States
                [3] 3Department of Psychiatry, VA Medical Center , Ann Arbor, MI, United States
                [4] 4Department of Psychiatry, University of Michigan , Ann Arbor, MI, United States
                Author notes

                Edited by: Martine Ammassari-Teule, Italian National Research Council (CNR), Italy

                Reviewed by: Pascale Gisquet-Verrier, Université Paris-Sud, France; Diego Andolina, Sapienza University of Rome, Italy

                *Correspondence: Lauren E. Chaby chaby@ 123456wayne.edu
                Article
                10.3389/fnbeh.2019.00024
                6406056
                30881293
                1c0ea54d-a7d3-436e-8cf4-f7b1c06e1ee3
                Copyright © 2019 Chaby, Karavidha, Lisieski, Perrine and Liberzon.

                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.

                History
                : 04 November 2018
                : 30 January 2019
                Page count
                Figures: 5, Tables: 2, Equations: 0, References: 96, Pages: 13, Words: 10710
                Funding
                Funded by: U.S. Department of Defense 10.13039/100000005
                Categories
                Neuroscience
                Original Research

                Neurosciences
                cognitive flexibility,dopamine,norepinephrine,single prolonged stress,trauma,ptsd
                Neurosciences
                cognitive flexibility, dopamine, norepinephrine, single prolonged stress, trauma, ptsd

                Comments

                Comment on this article