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      Behavioral Senescence and Aging-Related Changes in Motor Neurons and Brain Neuromodulator Levels Are Ameliorated by Lifespan-Extending Reproductive Dormancy in Drosophila

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          Abstract

          The lifespan of Drosophila melanogaster can be extended substantially by inducing reproductive dormancy (also known as diapause) by lowered temperature and short days. This increase of longevity is accompanied by lowered metabolism and increased stress tolerance. We ask here whether behavioral senescence is ameliorated during adult dormancy. To study this we kept flies for seven or more weeks in normal rearing conditions or in diapause conditions and compared to 1-week-old flies in different behavioral assays of sleep, negative geotaxis and exploratory walking. We found that the senescence of geotaxis and locomotor behavior seen under normal rearing conditions was negligible in flies kept in dormancy. The normal senescence of rhythmic activity and sleep patterns during the daytime was also reduced by adult dormancy. Investigating the morphology of specific neuromuscular junctions (NMJs), we found that changes normally seen with aging do not take place in dormant flies. To monitor age-associated changes in neuronal circuits regulating activity rhythms, sleep and walking behavior we applied antisera to tyrosine hydroxylase (TH), serotonin and several neuropeptides to examine changes in expression levels and neuron morphology. In most neuron types the levels of stored neuromodulators decreased during normal aging, but not in diapause treated flies. No signs of neurodegeneration were seen in either condition. Our data suggest that age-related changes in motor neurons could be the cause of part of the behavioral senescence and that this is ameliorated by reproductive diapause. Earlier studies established a link between age-associated decreases in neuromodulator levels and behavioral decline that could be rescued by overexpression of neuromodulator. Thus, it is likely that the retained levels of neuromodulators in dormant flies alleviate behavioral senescence.

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          Extension of life-span by loss of CHICO, a Drosophila insulin receptor substrate protein.

          The Drosophila melanogaster gene chico encodes an insulin receptor substrate that functions in an insulin/insulin-like growth factor (IGF) signaling pathway. In the nematode Caenorhabditis elegans, insulin/IGF signaling regulates adult longevity. We found that mutation of chico extends fruit fly median life-span by up to 48% in homozygotes and 36% in heterozygotes. Extension of life-span was not a result of impaired oogenesis in chico females, nor was it consistently correlated with increased stress resistance. The dwarf phenotype of chico homozygotes was also unnecessary for extension of life-span. The role of insulin/IGF signaling in regulating animal aging is therefore evolutionarily conserved.
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            • Record: found
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            • Article: not found

            Mushroom body memoir: from maps to models.

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

              The plasticity of aging: insights from long-lived mutants.

              Mutations in genes affecting endocrine signaling, stress responses, metabolism, and telomeres can all increase the life spans of model organisms. These mutations have revealed evolutionarily conserved pathways for aging, some of which appear to extend life span in response to sensory cues, caloric restriction, or stress. Many mutations affecting longevity pathways delay age-related disease, and the molecular analysis of these pathways is leading to a mechanistic understanding of how these two processes--aging and disease susceptibility--are linked.
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                Author and article information

                Contributors
                Journal
                Front Cell Neurosci
                Front Cell Neurosci
                Front. Cell. Neurosci.
                Frontiers in Cellular Neuroscience
                Frontiers Media S.A.
                1662-5102
                20 April 2017
                2017
                : 11
                : 111
                Affiliations
                [1] 1Department of Zoology, Stockholm University Stockholm, Sweden
                [2] 2Division of Biomedical and Life Sciences, Faculty of Health and Medicine, Lancaster University Lancaster, UK
                Author notes

                Edited by: Dieter Wicher, Max Planck Institute for Chemical Ecology (MPG), Germany

                Reviewed by: Timothy Mosca, Thomas Jefferson University, USA; Sofía Lavista Llanos, Max Planck Institute for Chemical Ecology (MPG), Germany

                *Correspondence: Dick R. Nässel dnassel@ 123456zoologi.su.se
                Article
                10.3389/fncel.2017.00111
                5408790
                28503133
                bb2f3b8f-4b44-4453-ae19-c00763fa51a7
                Copyright © 2017 Liao, Broughton and Nässel.

                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) or licensor 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
                : 13 February 2017
                : 03 April 2017
                Page count
                Figures: 9, Tables: 2, Equations: 0, References: 94, Pages: 20, Words: 13973
                Funding
                Funded by: Vetenskapsrà¥det 10.13039/501100004359
                Award ID: 621-2010-5742 and 2015-04626
                Award ID: KAW2012.0058
                Categories
                Neuroscience
                Original Research

                Neurosciences
                diapause,aging,sleep,negative geotaxis,walking behavior,insulin signaling,neuropeptides,dopamine
                Neurosciences
                diapause, aging, sleep, negative geotaxis, walking behavior, insulin signaling, neuropeptides, dopamine

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