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      Pulsed EMF stimulation increased BDNF and activated S6 levels in the hippocampus of senescent rats

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          Abstract

          Purpose

          Low-frequency electromagnetic field (EMF) exposure in rat has positive effects on neuronal processes in vitro. Moreover, EMF improves learning-memory and psychomotor activity during advanced ageing, but the underlying molecular mechanisms are not known in the brain. In the present study we aimed to investigate the molecular effects of chronic EMF stimulation in the hippocampus of senescent rats in vivo.

          Materials/Methods

          Thirty months old rats were treated for six weeks with different EMF doses of 45, 95, and 1,250 µT. After sacrifice the levels of Brain Derived Neurotrophic Factor (BDNF) and activated ribosomal protein S6 as measures for protein synthesis intensity in the hippocampus were determined by Western blot analysis.

          Results

          The results showed that chronic EMF exposure dose dependently increased BDNF and the amount of phosphorylated S6 protein at the highest dose. The effects on the two proteins positively correlated at individual level. The results indicate that EMF exposure may enhance neurotrophic processes indicated by increased BDNF expression in the hippocampus of senescent rats. Increased phosphorylated S6 protein suggests coupling to support molecular regulation of protein synthesis.

          Conclusions

          In a broader perspective, these findings may support EMF as a beneficial alternative form of passive exercise in active, exercise-limited, aged individuals.

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          Most cited references18

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          BDNF and 5-HT: a dynamic duo in age-related neuronal plasticity and neurodegenerative disorders.

          Brain-derived neurotrophic factor (BDNF) and serotonin (5-hydroxytryptamine, 5-HT) are known to regulate synaptic plasticity, neurogenesis and neuronal survival in the adult brain. These two signals co-regulate one another such that 5-HT stimulates the expression of BDNF, and BDNF enhances the growth and survival of 5-HT neurons. Impaired 5-HT and BDNF signaling is central to depression and anxiety disorders, but could also play important roles in the pathogenesis of several age-related disorders, including insulin resistance syndrome, Alzheimer's disease and Huntington's disease. Enhancement of BDNF signaling may be a key mechanism whereby cognitive stimulation, exercise, dietary restriction and antidepressant drugs preserve brain function during aging. Behavioral and pharmacological manipulations that enhance 5-HT and BDNF signaling could help promote healthy brain aging.
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            Translational control by MAPK signaling in long-term synaptic plasticity and memory.

            Enduring forms of synaptic plasticity and memory require new protein synthesis, but little is known about the underlying regulatory mechanisms. Here, we investigate the role of MAPK signaling in these processes. Conditional expression of a dominant-negative form of MEK1 in the postnatal murine forebrain inhibited ERK activation and caused selective deficits in hippocampal memory retention and the translation-dependent, transcription-independent phase of hippocampal L-LTP. In hippocampal neurons, ERK inhibition blocked neuronal activity-induced translation as well as phosphorylation of the translation factors eIF4E, 4EBP1, and ribosomal protein S6. Correspondingly, protein synthesis and translation factor phosphorylation induced in control hippocampal slices by L-LTP-generating tetanization were significantly reduced in mutant slices. Translation factor phosphorylation induced in the control hippocampus by memory formation was similarly diminished in the mutant hippocampus. These results suggest a crucial role for translational control by MAPK signaling in long-lasting forms of synaptic plasticity and memory.
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              The aging hippocampus: interactions between exercise, depression, and BDNF.

              Late adulthood is associated with increased hippocampal atrophy and dysfunction. Although there are multiple paths by which hippocampal deterioration occurs in late life, the authors discuss the evidence that a single nucleotide polymorphism in the brain-derived neurotrophic factor (BDNF) gene and age-related changes in BDNF protein or receptor expression contribute to hippocampal atrophy. The authors conclude that few studies have tested whether BDNF mediates age-related hippocampal atrophy and memory impairment. However, there is strong evidence that decreased BDNF is associated with age-related hippocampal dysfunction, memory impairment, and increased risk for depression, whereas increasing BDNF by aerobic exercise appears to ameliorate hippocampal atrophy, improve memory function, and reduce depression. Importantly, the most consistent associations between BDNF and hippocampal dysfunction have emerged from research on BDNF protein expression in rodents and serum and plasma concentrations of BDNF in humans. Current research suggests that the BDNF val66met polymorphism may be only weakly associated with hippocampal atrophy in late adulthood. These conclusions are interpreted in relation to age-related memory impairment and preventions for hippocampal atrophy.
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                Author and article information

                Contributors
                Journal
                2066
                Developments in Health Sciences
                DHS
                Akadémiai Kiadó (Budapest )
                2630-9378
                2630-936X
                20 October 2021
                10 February 2022
                : 4
                : 1
                : 7-10
                Affiliations
                [1 ] Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University , Budapest, Hungary
                [2 ] Research Center for Molecular Exercise Science, University of Physical Education , Budapest, Hungary
                [3 ] Groningen Institute for Evolutionary Life Sciences (GELIFES), Department of Molecular Neurobiology, University of Groningen , Groningen, The Netherlands
                Author notes
                [* ]Corresponding author. Department of Morphology and Physiology, Faculty of Health Sciences, Semmelweis University , H–1088, Vas u. 17, Budapest, Hungary. E-mail: nyakas.csaba@ 123456se-etk.hu
                Author information
                https://orcid.org/0000-0003-3756-0186
                Article
                10.1556/2066.2021.00043
                27dd196c-9f88-4bbd-a09b-039ea1e7d8f4
                © 2021 The Author(s)

                Open Access. This is an open-access article distributed under the terms of the Creative Commons Attribution 4.0 International License ( https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited, a link to the CC License is provided, and changes – if any – are indicated. (SID_1)

                History
                : 29 June 2021
                : 27 July 2021
                Page count
                Figures: 2, Equations: 0, References: 18, Pages: 04
                Funding
                Funded by: Semmelweis University
                Funded by: National Bionics Program
                Award ID: ED_17-1-2017-0009
                Custom metadata
                1

                Medicine,Immunology,Health & Social care,Microbiology & Virology,Infectious disease & Microbiology
                S6,senescent age,hippocampus,EMF stimulation,BDNF

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