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

      Vasopressin Signal Inhibition in Aged Mice Decreases Mortality under Chronic Jet Lag

      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.

          Summary

          Chronic jet lag, a model of shiftwork, increases mortality in aged mice. One potential reason for this association is that the chronic desynchronization between the internal clock phase and the environmental light/dark (LD) cycle might increase the mortality rate. However, this hypothesis has not been examined because of the lack of an appropriate animal model to prove this speculation. Here, we found that rapidly entrainable vasopressin receptor V1a –/– V1b –/– mice showed lower mortality under a chronic jet lag condition. Moreover, we found that pharmacological inactivation of V1a and V1b signaling decreased mortality even in aged wild-type mice, thus providing a potential pharmaceutical intervention for shiftwork-related health problems.

          Graphical Abstract

          Highlights

          • Chronic jet lag increases mortality in aged mice

          • Rapidly resetting V1a –/– V1b –/– mice showed lower mortality under chronic jet lag

          • Pharmacological inactivation of V1a/V1b signaling decreased mortality in aged WT mice

          • A potential pharmaceutical intervention for shiftwork-related health problems

          Abstract

          Human Activity in Medical Context; Neuroscience; Behavioral Neuroscience

          Related collections

          Most cited references15

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

          The genetics of mammalian circadian order and disorder: implications for physiology and disease.

          Circadian cycles affect a variety of physiological processes, and disruptions of normal circadian biology therefore have the potential to influence a range of disease-related pathways. The genetic basis of circadian rhythms is well studied in model organisms and, more recently, studies of the genetic basis of circadian disorders has confirmed the conservation of key players in circadian biology from invertebrates to humans. In addition, important advances have been made in understanding how these molecules influence physiological functions in tissues throughout the body. Together, these studies set the scene for applying our knowledge of circadian biology to the understanding and treatment of a range of human diseases, including cancer and metabolic and behavioural disorders.
            Bookmark
            • Record: found
            • Abstract: not found
            • Article: not found

            Loss of a circadian adrenal corticosterone rhythm following suprachiasmatic lesions in the rat.

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

              Circadian rhythms in drinking behavior and locomotor activity of rats are eliminated by hypothalamic lesions.

              Bilateral electrolytic lesions in the suprachiasmatic nuclei permanently eliminated nocturnal and circadian rhythms in drinking behavior and locomotor activity of albino rats. The generation of 24-hr behavioral rhythms and the entrainment of these rhythms to the light-dark cycle of environmental illumination may be coordinated by neurons in the suprachiasmatic region of the rat brain. Destruction of the medial preoptic area had no effect on 24-hr drinking rhythms.
                Bookmark

                Author and article information

                Contributors
                Journal
                iScience
                iScience
                iScience
                Elsevier
                2589-0042
                18 July 2018
                27 July 2018
                18 July 2018
                : 5
                : 118-122
                Affiliations
                [1 ]Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan
                Author notes
                []Corresponding author okamurah@ 123456pharm.kyoto-u.ac.jp
                [2]

                Lead Contact

                Article
                S2589-0042(18)30084-1
                10.1016/j.isci.2018.06.008
                6123867
                72da193c-b0ba-480e-b4b3-e1773b8679e5
                © 2018 The Author(s)

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 28 March 2018
                : 31 May 2018
                : 19 June 2018
                Categories
                Article

                human activity in medical context,neuroscience,behavioral neuroscience

                Comments

                Comment on this article