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

      Memory Impairment Induced by Chronic Psychosocial Stress Is Prevented by L-Carnitine

      Read this article at

      ScienceOpenPublisherPMC
      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

          Introduction

          Psychosocial stress (STS) negatively influences memory. This might be associated to oxidative stress-induced progressive destruction of numerous brain structures and functions. L-carnitine (L-CAR) is a widely used antioxidant compound that is endogenously made in mammalian species. The current study investigated the effect of L-CAR on STS-induced memory impairment in the rat hippocampus.

          Methods

          The STS was induced using intruder model, where two rats were randomly switched from each one cage to another, once/day for 6 weeks. Concurrently, L-CAR (300mg/kg/day) was intraperitoneally administered for 6 weeks. After that, radial arm water maze (RAWM) was used to assess spatial learning memory in rats. Hippocampal biomarkers of oxidative stress, including thiobarbituric acid reactive substance (TBARs), oxidized glutathione (GSSG), reduced glutathione (GSH), glutathione peroxidase (GPx), catalase, and superoxide dismutase (SOD), and Brain-derived neurotrophic factor (BDNF) were examined.

          Results

          The results showed impairment of short-term memory (P < 0.05) during STS, whereas L-CAR treatment protected against this effect. Furthermore, while no change was observed in GSH, GSSG, GPx, catalase, and SOD, L-carnitine normalized STS-induced reduction in the hippocampal BDNF levels and increase in TBARS levels.

          Discussion

          Chronic psychosocial stress-induced memory impairment was prevented via L-CAR administration, which could have been achieved via normalizing changes in lipid peroxidation (TBARs) and BDNF levels in the hippocampus.

          Related collections

          Most cited references 47

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

          Alterations of serum levels of brain-derived neurotrophic factor (BDNF) in depressed patients with or without antidepressants.

          Because researchers have reported that antidepressants increase the expression of brain-derived neurotrophic factor (BDNF) in the rat hippocampus, we investigated whether serum BDNF levels may be used as a putative biological marker for major depressive disorders (MDD). We measured serum BDNF in the following three groups: antidepressant-naive patients with MDD (n = 16), antidepressant-treated patients with MDD (n = 17), and normal control subjects (n = 50). Patients were evaluated using the Hamilton Rating Scale for Depression (HAM-D). Serum BDNF was assayed with the sandwich ELISA method. We found that serum BDNF was significantly lower in the antidepressant-naive group (mean, 17.6 ng/mL; SD, 9.6) than in the treated (mean, 30.6 ng/mL; SD, 12.3; p =.001) or in the control group (mean, 27.7 ng/mL; SD, 11.4; p =.002). There was a significant negative correlation (r = -.350, z = -2.003, p =.045) between serum BDNF and HAM-D scores in all patients. In a preliminary examination, reduced BDNF values of three drug-naive patients recovered to basal levels after antidepressant treatment. Our study suggests that low BDNF levels may play a pivotal role in the pathophysiology of MDD and that antidepressants may increase BDNF in depressed patients.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Chronic stress, as well as acute stress, reduces BDNF mRNA expression in the rat hippocampus but less robustly.

            Daily restraint for 3 weeks was shown to atrophy dendrites of hippocampal pyramidal neurons in rats. Brain-derived neurotrophic factor (BDNF), which maintains neuronal survival and morphology, has been shown to decrease in response to acute stress. Plasma glucocorticoid (GC) and serotonergic projections from the raphe nuclei play major roles in reducing BDNF synthesis in the hippocampus. We investigated BDNF mRNA levels there, together with plasma GC levels, GC receptors in the hippocampus/hypothalamus and 5-HT synthesizing enzyme, tryptophan hydroxylase in the raphe nuclei, in animals chronically stressed for 1-3 weeks, using in situ hybridization and immunohistochemistry. In these animals, BDNF mRNA levels were significantly decreased in the hippocampus after 6 h of restraint, but the ability of restraint to reduce BDNF synthesis seemed less robust than that seen in acute stress models. HPA axis response to stress in these animals assessed by plasma GC levels was delayed and sustained, and the GC receptor in the paraventricular hypothalamic nucleus was increased at 1 week. Tryptophan hydroxylase immunoreactivity was increased in the median raphe nucleus at 2-3 weeks. Repetitive stress-induced reduction of BDNF may partly contribute to the neuronal atrophy/death and reduction of hippocampal volume observed both in animals and humans suffering chronic stress and/or depression.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Anti-oxidative effects of curcumin on immobilization-induced oxidative stress in rat brain, liver and kidney.

              Restraint stress has been indicated to induce oxidative damage in tissues. Several investigations have reported that curcumin (CUR) may have a protective effect against oxidative stress. The present study was designed to investigate the protective effects of CUR on restraint stress induced oxidative stress damage in the brain, liver and kidneys. For chronic restraint stress, rats were kept in the restrainers for 1h every day, for 21 consecutive days. The animals received systemic administrations of CUR daily for 21days. In order to evaluate the changes of the oxidative stress parameters following restraint stress, the levels of malondialdehyde (MDA), reduced glutathione (GSH), as well as antioxidant enzyme activities superoxide dismutase (SOD) glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CAT) were measured in the brain, liver and kidney of rats after the end of restraint stress. The restraint stress significantly increased MDA level, but decreased the level of GSH and activists of SOD, GPx, GR, and CAT the brain, liver and kidney of rats in comparison to the normal rats (P<0.001). Intraperitoneal administration of CUR significantly attenuated oxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in the tissues versus the control group (P<0.05). This study shows that CUR can prevent restraint stress-induced oxidative damage in the brain, liver and kidney of rats and propose that CUR may be useful agents against oxidative stress in the tissues.
                Bookmark

                Author and article information

                Journal
                Drug Des Devel Ther
                Drug Des Devel Ther
                DDDT
                dddt
                Drug Design, Development and Therapy
                Dove
                1177-8881
                19 December 2019
                2019
                : 13
                : 4341-4350
                Affiliations
                [1 ]Department of Biological Sciences, School of Science, The University of Jordan , Amman 11942, Jordan
                [2 ]Department of Medical Science, Irbid Faculty, Al-Balqa Applied University (BAU) , Irbid 21110, Jordan
                [3 ]Department of Clinical Pharmacy, Jordan University of Science and Technology , Irbid 22110, Jordan
                [4 ]Department of Biology, Yarmouk University , Irbid 21163, Jordan
                [5 ]Department of Neurosciences, Jordan University of Science and Technology , Irbid 22110, Jordan
                Author notes
                Correspondence: Karem H Alzoubi Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology , PO Box 3030, Irbid22110, JordanTel +962 2 7201000/ext. 23521Fax +962 2 7201075 Email khalzoubi@just.edu.jo
                Article
                225264
                10.2147/DDDT.S225264
                6927795
                © 2019 Rababa’h 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. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 5, References: 52, Pages: 10
                Categories
                Original Research

                Comments

                Comment on this article