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Iron entry in neurons and astrocytes: a link with synaptic activity
Iron plays a fundamental role in the development of the central nervous system (CNS) as well as in several neuronal functions including synaptic plasticity. Accordingly, neuronal iron supply is tightly controlled: it depends not only on transferrin-bound iron but also on non-transferrin-bound iron (...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Frontiers Media S.A.
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452822/ https://www.ncbi.nlm.nih.gov/pubmed/26089776 http://dx.doi.org/10.3389/fnmol.2015.00018 |
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author | Codazzi, Franca Pelizzoni, Ilaria Zacchetti, Daniele Grohovaz, Fabio |
author_facet | Codazzi, Franca Pelizzoni, Ilaria Zacchetti, Daniele Grohovaz, Fabio |
author_sort | Codazzi, Franca |
collection | PubMed |
description | Iron plays a fundamental role in the development of the central nervous system (CNS) as well as in several neuronal functions including synaptic plasticity. Accordingly, neuronal iron supply is tightly controlled: it depends not only on transferrin-bound iron but also on non-transferrin-bound iron (NTBI), which represents a relevant quote of the iron physiologically present in the cerebrospinal fluid (CSF). Different calcium permeable channels as well as the divalent metal transporter 1 (DMT1) have been proposed to sustain NTBI entry in neurons and astrocytes even though it remains an open issue. In both cases, it emerges that the control of iron entry is tightly linked to synaptic activity. The iron-induced oxidative tone can, in physiological conditions, positively influence the calcium levels and thus the synaptic plasticity. On the other hand, an excess of iron, with the ensuing uncontrolled production of reactive oxygen species (ROS), is detrimental for neuronal survival. A protective mechanism can be played by astrocytes that, more resistant to oxidative stress, can uptake iron, thereby buffering its concentration in the synaptic environment. This competence is potentiated when astrocytes undergo activation during neuroinflammation and neurodegenerative processes. In this minireview we focus on the mechanisms responsible for NTBI entry in neurons and astrocytes and on how they can be modulated during synaptic activity. Finally, we speculate on the relevance they may have in both physiological and pathological conditions. |
format | Online Article Text |
id | pubmed-4452822 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-44528222015-06-18 Iron entry in neurons and astrocytes: a link with synaptic activity Codazzi, Franca Pelizzoni, Ilaria Zacchetti, Daniele Grohovaz, Fabio Front Mol Neurosci Neuroscience Iron plays a fundamental role in the development of the central nervous system (CNS) as well as in several neuronal functions including synaptic plasticity. Accordingly, neuronal iron supply is tightly controlled: it depends not only on transferrin-bound iron but also on non-transferrin-bound iron (NTBI), which represents a relevant quote of the iron physiologically present in the cerebrospinal fluid (CSF). Different calcium permeable channels as well as the divalent metal transporter 1 (DMT1) have been proposed to sustain NTBI entry in neurons and astrocytes even though it remains an open issue. In both cases, it emerges that the control of iron entry is tightly linked to synaptic activity. The iron-induced oxidative tone can, in physiological conditions, positively influence the calcium levels and thus the synaptic plasticity. On the other hand, an excess of iron, with the ensuing uncontrolled production of reactive oxygen species (ROS), is detrimental for neuronal survival. A protective mechanism can be played by astrocytes that, more resistant to oxidative stress, can uptake iron, thereby buffering its concentration in the synaptic environment. This competence is potentiated when astrocytes undergo activation during neuroinflammation and neurodegenerative processes. In this minireview we focus on the mechanisms responsible for NTBI entry in neurons and astrocytes and on how they can be modulated during synaptic activity. Finally, we speculate on the relevance they may have in both physiological and pathological conditions. Frontiers Media S.A. 2015-06-03 /pmc/articles/PMC4452822/ /pubmed/26089776 http://dx.doi.org/10.3389/fnmol.2015.00018 Text en Copyright © 2015 Codazzi, Pelizzoni, Zacchetti and Grohovaz. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution and 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. |
spellingShingle | Neuroscience Codazzi, Franca Pelizzoni, Ilaria Zacchetti, Daniele Grohovaz, Fabio Iron entry in neurons and astrocytes: a link with synaptic activity |
title | Iron entry in neurons and astrocytes: a link with synaptic activity |
title_full | Iron entry in neurons and astrocytes: a link with synaptic activity |
title_fullStr | Iron entry in neurons and astrocytes: a link with synaptic activity |
title_full_unstemmed | Iron entry in neurons and astrocytes: a link with synaptic activity |
title_short | Iron entry in neurons and astrocytes: a link with synaptic activity |
title_sort | iron entry in neurons and astrocytes: a link with synaptic activity |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4452822/ https://www.ncbi.nlm.nih.gov/pubmed/26089776 http://dx.doi.org/10.3389/fnmol.2015.00018 |
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