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      Pain aversion and anxiety-like behavior occur at different times during the course of chronic inflammatory pain in rats

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          Abstract

          Pain is considered a multidimensional conscious experience that includes a sensory component and a negative affective-motivational component. The negative affective-motivational component of pain is different from the sensory component and amplifies the pain experience. Nowadays, a significant number of preclinical research groups have focused their attention on the affective symptoms of pain. In the present study, we investigated the pain aversion and anxiety-like behavior of the complete Freund’s adjuvant (CFA)-induced chronic pain model. CFA rats experienced spontaneous pain during pain-paired conditioning (pain aversion) and spontaneous pain produces an affective response (anxiety-like behavior). Moreover, pain aversion was gradually attenuated, while the anxiety-like behavior increased in 4 weeks. Therefore, although the negative effect (including pain aversion and anxiety) is always associated with hyperalgesia, the manifestations of negative effect may follow different time courses, which may influence the progress of primary disease. The findings illustrate that targeted therapy should focus on a specific aspect in different stages of pain. Our study emphasizes the necessity of using multiple tests to study pain comorbidities.

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          Most cited references 28

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          Emotional behavior in the rat. I. Defecation and urination as measures of individual differences in emotionality.

           C S Hall (1934)
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            Fifteen Years of Explaining Pain: The Past, Present, and Future.

            The pain field has been advocating for some time for the importance of teaching people how to live well with pain. Perhaps some, and maybe even for many, we might again consider the possibility that we can help people live well without pain. Explaining Pain (EP) refers to a range of educational interventions that aim to change one's understanding of the biological processes that are thought to underpin pain as a mechanism to reduce pain itself. It draws on educational psychology, in particular conceptual change strategies, to help patients understand current thought in pain biology. The core objective of the EP approach to treatment is to shift one's conceptualization of pain from that of a marker of tissue damage or disease to that of a marker of the perceived need to protect body tissue. Here, we describe the historical context and beginnings of EP, suggesting that it is a pragmatic application of the biopsychosocial model of pain, but differentiating it from cognitive behavioral therapy and educational components of early multidisciplinary pain management programs. We attempt to address common misconceptions of EP that have emerged over the last 15 years, highlighting that EP is not behavioral or cognitive advice, nor does it deny the potential contribution of peripheral nociceptive signals to pain. We contend that EP is grounded in strong theoretical frameworks, that its targeted effects are biologically plausible, and that available behavioral evidence is supportive. We update available meta-analyses with results of a systematic review of recent contributions to the field and propose future directions by which we might enhance the effects of EP as part of multimodal pain rehabilitation. Perspective: EP is a range of educational interventions. EP is grounded in conceptual change and instructional design theory. It increases knowledge of pain-related biology, decreases catastrophizing, and imparts short-term reductions in pain and disability. It presents the biological information that justifies a biopsychosocial approach to rehabilitation.
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              Behavioural and pharmacological characterisation of the elevated "zero-maze" as an animal model of anxiety.

              The elevated "zero-maze" is a modification of the elevated plus-maze model of anxiety in rats which incorporates both traditional and novel ethological measures in the analysis of drug effects. The novel design comprises an elevated annular platform with two opposite enclosed quadrants and two open, removing any ambiguity in interpretation of time spent on the central square of the traditional design and allowing uninterrupted exploration. Using this model, the reference benzodiazepine anxiolytics, diazepam (0.125-0.5 mg/kg) and chlordiazepoxide (0.5-2.0 mg/kg) significantly increased the percentage of time spent in the open quadrants (% TO) and the frequency of head dips over the edge of the platform (HDIPS), and reduced the frequency of stretched attend postures (SAP) from the closed to open quadrants. In contrast, the anxiogenic drug m-chlorophenyl-piperazine (mCPP; 0.25-1.0 mg/kg) induced the opposite effects, decreasing %TO and HDIPS, and increasing SAP. The 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT; 0.001-0.1 mg/kg) had no effects on either %TO or HDIPS, but did decrease SAP at 0.01 mg/kg although not at higher or lower doses. Similarly, the 5-HT3 receptor antagonist, ondansetron (0.0001-1.0 mg/kg) decreased SAP and increased %TO at 0.01 mg/kg, but not at other doses. The present data suggest that a combination of the novel "zero-maze" design and a detailed ethological analysis provides a sensitive model for the detection of anxiolytic/anxiogenic drug action.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                Journal of Pain Research
                Journal of Pain Research
                Dove Medical Press
                1178-7090
                2017
                06 November 2017
                : 10
                : 2585-2593
                Affiliations
                [1 ]Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, Hangzhou
                [2 ]The Third Affiliated Hospital of Zhejiang Chinese Medical University, Zhejiang, China
                Author notes
                Correspondence: Jianqiao Fang, Department of Neurobiology and Acupuncture Research, The Third Clinical Medical College, Zhejiang Chinese Medical University, 548 Binwen Road, Binjiang District, Hangzhou, Zhejiang 310053, China, Tel +86 571 8667 3000, Email fangjianqiao7532@ 123456163.com
                Article
                jpr-10-2585
                10.2147/JPR.S139679
                5683785
                © 2017 Wu et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Original Research

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