Role of astrocytes in manganese mediated neurotoxicity
Astrocytes are responsible for numerous aspects of metabolic support, nutrition, control of the ion and neurotransmitter environment in central nervous system (CNS). Failure by astrocytes to support essential neuronal metabolic requirements plays a fundamental role in the pathogenesis of brain injur...
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| Veröffentlicht in: | BMC pharmacology & toxicology 2013-04, Vol.14 (1), p.23-23, Article 23 |
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| creator | Sidoryk-Wegrzynowicz, Marta Aschner, Michael |
| description | Astrocytes are responsible for numerous aspects of metabolic support, nutrition, control of the ion and neurotransmitter environment in central nervous system (CNS). Failure by astrocytes to support essential neuronal metabolic requirements plays a fundamental role in the pathogenesis of brain injury and the ensuing neuronal death. Astrocyte-neuron interactions play a central role in brain homeostasis, in particular via neurotransmitter recycling functions. Disruption of the glutamine (Gln)/glutamate (Glu) -γ-aminobutyric acid (GABA) cycle (GGC) between astrocytes and neurons contributes to changes in Glu-ergic and/or GABA-ergic transmission, and is associated with several neuropathological conditions, including manganese (Mn) toxicity. In this review, we discuss recent advances in support of the important roles for astrocytes in normal as well as neuropathological conditions primarily those caused by exposure to Mn. |
| doi_str_mv | 10.1186/2050-6511-14-23 |
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Failure by astrocytes to support essential neuronal metabolic requirements plays a fundamental role in the pathogenesis of brain injury and the ensuing neuronal death. Astrocyte-neuron interactions play a central role in brain homeostasis, in particular via neurotransmitter recycling functions. Disruption of the glutamine (Gln)/glutamate (Glu) -γ-aminobutyric acid (GABA) cycle (GGC) between astrocytes and neurons contributes to changes in Glu-ergic and/or GABA-ergic transmission, and is associated with several neuropathological conditions, including manganese (Mn) toxicity. In this review, we discuss recent advances in support of the important roles for astrocytes in normal as well as neuropathological conditions primarily those caused by exposure to Mn.</description><identifier>ISSN: 2050-6511</identifier><identifier>EISSN: 2050-6511</identifier><identifier>DOI: 10.1186/2050-6511-14-23</identifier><identifier>PMID: 23594835</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Apoptosis ; Astrocytes ; Astrocytes - metabolism ; Brain ; Brain injury ; Cell death ; Central nervous system ; Dissolved organic carbon ; Enzymes ; GABA ; Glutamate ; Glutamic Acid - metabolism ; Glutamine ; Glutamine - metabolism ; Head injuries ; Homeostasis ; Humans ; Injuries ; Kinases ; Manganese ; Manganese - toxicity ; Metabolism ; Metabolites ; Neurons ; Neurophysiology ; Neurotoxicity ; Neurotoxicity Syndromes - etiology ; Neurotoxicity Syndromes - metabolism ; Neurotransmitters ; Nutrition ; Pathogenesis ; Proteins ; Review ; Toxicity ; γ-Aminobutyric acid</subject><ispartof>BMC pharmacology & toxicology, 2013-04, Vol.14 (1), p.23-23, Article 23</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Sidoryk-Wegrzynowicz and Aschner; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Sidoryk-Wegrzynowicz and Aschner; licensee BioMed Central Ltd. 2013 Sidoryk-Wegrzynowicz and Aschner; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b578t-d929f51ae738e180191d85ba97a5f0cea80ca511b851313aee01bc1faa8382d93</citedby><cites>FETCH-LOGICAL-b578t-d929f51ae738e180191d85ba97a5f0cea80ca511b851313aee01bc1faa8382d93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637816/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3637816/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27922,27923,53789,53791</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23594835$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sidoryk-Wegrzynowicz, Marta</creatorcontrib><creatorcontrib>Aschner, Michael</creatorcontrib><title>Role of astrocytes in manganese mediated neurotoxicity</title><title>BMC pharmacology & toxicology</title><addtitle>BMC Pharmacol Toxicol</addtitle><description>Astrocytes are responsible for numerous aspects of metabolic support, nutrition, control of the ion and neurotransmitter environment in central nervous system (CNS). Failure by astrocytes to support essential neuronal metabolic requirements plays a fundamental role in the pathogenesis of brain injury and the ensuing neuronal death. Astrocyte-neuron interactions play a central role in brain homeostasis, in particular via neurotransmitter recycling functions. Disruption of the glutamine (Gln)/glutamate (Glu) -γ-aminobutyric acid (GABA) cycle (GGC) between astrocytes and neurons contributes to changes in Glu-ergic and/or GABA-ergic transmission, and is associated with several neuropathological conditions, including manganese (Mn) toxicity. In this review, we discuss recent advances in support of the important roles for astrocytes in normal as well as neuropathological conditions primarily those caused by exposure to Mn.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Astrocytes</subject><subject>Astrocytes - metabolism</subject><subject>Brain</subject><subject>Brain injury</subject><subject>Cell death</subject><subject>Central nervous system</subject><subject>Dissolved organic carbon</subject><subject>Enzymes</subject><subject>GABA</subject><subject>Glutamate</subject><subject>Glutamic Acid - metabolism</subject><subject>Glutamine</subject><subject>Glutamine - metabolism</subject><subject>Head injuries</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Injuries</subject><subject>Kinases</subject><subject>Manganese</subject><subject>Manganese - toxicity</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Neurons</subject><subject>Neurophysiology</subject><subject>Neurotoxicity</subject><subject>Neurotoxicity Syndromes - etiology</subject><subject>Neurotoxicity Syndromes - metabolism</subject><subject>Neurotransmitters</subject><subject>Nutrition</subject><subject>Pathogenesis</subject><subject>Proteins</subject><subject>Review</subject><subject>Toxicity</subject><subject>γ-Aminobutyric acid</subject><issn>2050-6511</issn><issn>2050-6511</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNp1ktFrFDEQxoMottQ--yYLgm_bZpLNbvZFqEVboSCIPofZ7Oxdym5SN9ni_ffmuHreQU0eEmZ-8_HNMIy9BX4BoOtLwRUvawVQQlUK-YKd7iMvD_4n7DzGe55P02itxGt2IqRqKy3VKau_h5GKMBQY0xzsJlEsnC8m9Cv0FKmYqHeYqC88LXNI4bezLm3esFcDjpHOn94z9vPL5x_Xt-Xdt5uv11d3Zacancq-Fe2gAKmRmkBzaKHXqsO2QTVwS6i5xWyx0wokSCTi0FkYELXUom_lGfu4031YuuzEkk8zjuZhdhPOGxPQmeOMd2uzCo9G1rLRUGeBTzuBzoX_CBxnbJjMdnRmOzoDlREyi7x_cjGHXwvFZO7DMvvceAZEXQle1fCPWuFIxvkhZEE7uWjNlZKVrngtq0xdPEPl29PkbPA0uBw_KvhwULAmHNM6hnFJLvh4DF7uQDuHGGca9l0CN9uFeaavd4fT3fN_10P-AZlhuUI</recordid><startdate>20130418</startdate><enddate>20130418</enddate><creator>Sidoryk-Wegrzynowicz, Marta</creator><creator>Aschner, Michael</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20130418</creationdate><title>Role of astrocytes in manganese mediated neurotoxicity</title><author>Sidoryk-Wegrzynowicz, Marta ; 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| subjects | Animals Apoptosis Astrocytes Astrocytes - metabolism Brain Brain injury Cell death Central nervous system Dissolved organic carbon Enzymes GABA Glutamate Glutamic Acid - metabolism Glutamine Glutamine - metabolism Head injuries Homeostasis Humans Injuries Kinases Manganese Manganese - toxicity Metabolism Metabolites Neurons Neurophysiology Neurotoxicity Neurotoxicity Syndromes - etiology Neurotoxicity Syndromes - metabolism Neurotransmitters Nutrition Pathogenesis Proteins Review Toxicity γ-Aminobutyric acid |
| title | Role of astrocytes in manganese mediated neurotoxicity |
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