Aging abolishes circadian rhythms and disrupts temporal organization of antioxidant-prooxidant status, endogenous clock activity and neurotrophin gene expression in the rat temporal cortex.

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  • Additional Information
    • Source:
      Publisher: Elsevier Science Country of Publication: United States NLM ID: 7605074 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7544 (Electronic) Linking ISSN: 03064522 NLM ISO Abbreviation: Neuroscience Subsets: MEDLINE
    • Publication Information:
      Publication: [New York?] : Elsevier Science
      Original Publication: Oxford, Elmsford, N. Y., Pergamon Press
    • Subject Terms:
      Aging*/metabolism ; Aging*/physiology ; Circadian Rhythm*/physiology ; Temporal Lobe*/metabolism ; CLOCK Proteins*/metabolism ; CLOCK Proteins*/genetics ; Rats, Wistar* ; ARNTL Transcription Factors*/metabolism ; ARNTL Transcription Factors*/genetics ; Oxidative Stress*/physiology ; Lipid Peroxidation*/physiology; Animals ; Male ; Rats ; Brain-Derived Neurotrophic Factor/metabolism ; Brain-Derived Neurotrophic Factor/genetics ; Antioxidants/metabolism ; Glutathione Peroxidase/metabolism ; Glutathione Peroxidase/genetics ; Nerve Growth Factors/metabolism ; Nerve Growth Factors/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 1/metabolism ; Nuclear Receptor Subfamily 1, Group F, Member 1/genetics ; Gene Expression
    • Abstract:
      Disruption of circadian rhythms contributes to deficits in cognitive functions during aging. Up to date, the biochemical, molecular and chronobiological bases of such deterioration have not been completely elucidated. Here, we aim: 1) to investigate the endogenous nature of 24 h-rhythms of antioxidant defenses, oxidative stress, clocḱ's, and neurotrophic factors expression, in the rat temporal cortex (TC), and 2) to study the consequences of aging on the circadian organization of those factors. We observed a circadian organization of antioxidant enzymes activity, lipoperoxidation and the clock, BMAL1 and RORa, proteins, in the TC of young rats. Such temporal organization suggests the existence of a two-way communication among clock transcription factors and antioxidant defenses. This might generate the rhythmic and circadian expression of Bdnf and Rc3 genes involved in the TC-depending cognitive function. Noteworthy, such circadian organization disappears in the TC of aged rats. Aging also reduces glutathione peroxidase activity and expression, and it increases lipid peroxidation, throughout a 24 h-period. An increased oxidative stress makes the cellular redox environment change into an oxidative status which alters the endogenous clock activity and disrupts the circadian organization of, at least part, of the molecular basis of the synaptic plasticity in the TC.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
      (Copyright © 2024 International Brain Research Organization (IBRO). Published by Elsevier Inc. All rights reserved.)
    • Contributed Indexing:
      Keywords: Aging; Antioxidant Enzyme; Bdnf; Circadian Rhythm; Rc3; Temporal Cortex
    • Accession Number:
      EC 2.3.1.48 (CLOCK Proteins)
      0 (ARNTL Transcription Factors)
      0 (Brain-Derived Neurotrophic Factor)
      0 (Antioxidants)
      EC 1.11.1.9 (Glutathione Peroxidase)
      0 (Nerve Growth Factors)
      0 (Arntl protein, rat)
      0 (Nuclear Receptor Subfamily 1, Group F, Member 1)
      EC 2.3.1.48 (Clock protein, rat)
    • Publication Date:
      Date Created: 20240907 Date Completed: 20241013 Latest Revision: 20241013
    • Publication Date:
      20241014
    • Accession Number:
      10.1016/j.neuroscience.2024.09.008
    • Accession Number:
      39244007