Calcium and glial cell death
Calcium (Ca 2+) homeostasis is crucial for development and survival of virtually all types of cells including glia of the central nervous system (CNS). Astrocytes, oligodendrocytes and microglia, the major glial cell types in the CNS, are endowed with a rather sophisticated array of Ca 2+-permeable...
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| Veröffentlicht in: | Cell calcium (Edinburgh) 2005-09, Vol.38 (3), p.417-425 |
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| container_title | Cell calcium (Edinburgh) |
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| creator | Alberdi, Elena Sánchez-Gómez, María Victoria Matute, Carlos |
| description | Calcium (Ca
2+) homeostasis is crucial for development and survival of virtually all types of cells including glia of the central nervous system (CNS). Astrocytes, oligodendrocytes and microglia, the major glial cell types in the CNS, are endowed with a rather sophisticated array of Ca
2+-permeable receptors and channels, as well as store-operated channels and pumps, all of which determine Ca
2+ homeostasis. In addition, glial cells detect functional activity in neighbouring neurons and respond to it by means of Ca
2+ signals that can modulate synaptic interactions. Like in neurons, Ca
2+ overload resulting from dysregulation of channels and pumps can be deleterious to glia. In this review, we summarize recent advances in the understanding Ca
2+ homeostasis in glial cells, the consequences of its alteration in cell demise as well as in neurological and psychiatric disorders that experience glial cell loss. |
| doi_str_mv | 10.1016/j.ceca.2005.06.020 |
| format | Article |
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2+) homeostasis is crucial for development and survival of virtually all types of cells including glia of the central nervous system (CNS). Astrocytes, oligodendrocytes and microglia, the major glial cell types in the CNS, are endowed with a rather sophisticated array of Ca
2+-permeable receptors and channels, as well as store-operated channels and pumps, all of which determine Ca
2+ homeostasis. In addition, glial cells detect functional activity in neighbouring neurons and respond to it by means of Ca
2+ signals that can modulate synaptic interactions. Like in neurons, Ca
2+ overload resulting from dysregulation of channels and pumps can be deleterious to glia. In this review, we summarize recent advances in the understanding Ca
2+ homeostasis in glial cells, the consequences of its alteration in cell demise as well as in neurological and psychiatric disorders that experience glial cell loss.</description><identifier>ISSN: 0143-4160</identifier><identifier>EISSN: 1532-1991</identifier><identifier>DOI: 10.1016/j.ceca.2005.06.020</identifier><identifier>PMID: 16095689</identifier><language>eng</language><publisher>Netherlands: Elsevier India Pvt Ltd</publisher><subject>Animals ; Apoptosis ; Apoptosis - physiology ; Calcium - physiology ; Calcium Channels - physiology ; Degeneration ; Excitotoxicity ; Homeostasis - physiology ; Humans ; Isquemia ; Mitochondria ; Neuroglia - physiology ; Reactive oxygen species</subject><ispartof>Cell calcium (Edinburgh), 2005-09, Vol.38 (3), p.417-425</ispartof><rights>2005 Elsevier Ltd</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c385t-c1963c761b9c513b951e0353b9d6ca2b4015d0c9b2c5ef3ccbbdae01b43bf4cd3</citedby><cites>FETCH-LOGICAL-c385t-c1963c761b9c513b951e0353b9d6ca2b4015d0c9b2c5ef3ccbbdae01b43bf4cd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.ceca.2005.06.020$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,777,781,3537,27905,27906,45976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16095689$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Alberdi, Elena</creatorcontrib><creatorcontrib>Sánchez-Gómez, María Victoria</creatorcontrib><creatorcontrib>Matute, Carlos</creatorcontrib><title>Calcium and glial cell death</title><title>Cell calcium (Edinburgh)</title><addtitle>Cell Calcium</addtitle><description>Calcium (Ca
2+) homeostasis is crucial for development and survival of virtually all types of cells including glia of the central nervous system (CNS). Astrocytes, oligodendrocytes and microglia, the major glial cell types in the CNS, are endowed with a rather sophisticated array of Ca
2+-permeable receptors and channels, as well as store-operated channels and pumps, all of which determine Ca
2+ homeostasis. In addition, glial cells detect functional activity in neighbouring neurons and respond to it by means of Ca
2+ signals that can modulate synaptic interactions. Like in neurons, Ca
2+ overload resulting from dysregulation of channels and pumps can be deleterious to glia. In this review, we summarize recent advances in the understanding Ca
2+ homeostasis in glial cells, the consequences of its alteration in cell demise as well as in neurological and psychiatric disorders that experience glial cell loss.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - physiology</subject><subject>Calcium - physiology</subject><subject>Calcium Channels - physiology</subject><subject>Degeneration</subject><subject>Excitotoxicity</subject><subject>Homeostasis - physiology</subject><subject>Humans</subject><subject>Isquemia</subject><subject>Mitochondria</subject><subject>Neuroglia - physiology</subject><subject>Reactive oxygen species</subject><issn>0143-4160</issn><issn>1532-1991</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkE1LxDAQhoMo7rr6B0SkJ2-tM02TbsCLLH7Bghc9h2SSapZ2q00r-O9t2QVveppheN6X4WHsHCFDQHm9yciTyXIAkYHMIIcDNkfB8xSVwkM2Byx4WqCEGTuJcQMAipd4zGbjSQm5VHN2sTI1haFJzNYlb3UwdUK-rhPnTf9-yo4qU0d_tp8L9np_97J6TNfPD0-r23VKfCn6lFBJTqVEq0ggt0qgBy7GxUkyuS0AhQNSNifhK05krTMe0BbcVgU5vmBXu96Prv0cfOx1E-L0htn6dohaLkWZF6X4F8RypHLFRzDfgdS1MXa-0h9daEz3rRH0JE9v9CRPT_I0SD3KG0OX-_bBNt79Rva2RuBmB_hRxlfwnY4U_Ja8C52nXrs2_NX_Azc-fgY</recordid><startdate>20050901</startdate><enddate>20050901</enddate><creator>Alberdi, Elena</creator><creator>Sánchez-Gómez, María Victoria</creator><creator>Matute, Carlos</creator><general>Elsevier India Pvt Ltd</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>7QP</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>20050901</creationdate><title>Calcium and glial cell death</title><author>Alberdi, Elena ; Sánchez-Gómez, María Victoria ; Matute, Carlos</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c385t-c1963c761b9c513b951e0353b9d6ca2b4015d0c9b2c5ef3ccbbdae01b43bf4cd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - physiology</topic><topic>Calcium - physiology</topic><topic>Calcium Channels - physiology</topic><topic>Degeneration</topic><topic>Excitotoxicity</topic><topic>Homeostasis - physiology</topic><topic>Humans</topic><topic>Isquemia</topic><topic>Mitochondria</topic><topic>Neuroglia - physiology</topic><topic>Reactive oxygen species</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Alberdi, Elena</creatorcontrib><creatorcontrib>Sánchez-Gómez, María Victoria</creatorcontrib><creatorcontrib>Matute, Carlos</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Cell calcium (Edinburgh)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Alberdi, Elena</au><au>Sánchez-Gómez, María Victoria</au><au>Matute, Carlos</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Calcium and glial cell death</atitle><jtitle>Cell calcium (Edinburgh)</jtitle><addtitle>Cell Calcium</addtitle><date>2005-09-01</date><risdate>2005</risdate><volume>38</volume><issue>3</issue><spage>417</spage><epage>425</epage><pages>417-425</pages><issn>0143-4160</issn><eissn>1532-1991</eissn><abstract>Calcium (Ca
2+) homeostasis is crucial for development and survival of virtually all types of cells including glia of the central nervous system (CNS). Astrocytes, oligodendrocytes and microglia, the major glial cell types in the CNS, are endowed with a rather sophisticated array of Ca
2+-permeable receptors and channels, as well as store-operated channels and pumps, all of which determine Ca
2+ homeostasis. In addition, glial cells detect functional activity in neighbouring neurons and respond to it by means of Ca
2+ signals that can modulate synaptic interactions. Like in neurons, Ca
2+ overload resulting from dysregulation of channels and pumps can be deleterious to glia. In this review, we summarize recent advances in the understanding Ca
2+ homeostasis in glial cells, the consequences of its alteration in cell demise as well as in neurological and psychiatric disorders that experience glial cell loss.</abstract><cop>Netherlands</cop><pub>Elsevier India Pvt Ltd</pub><pmid>16095689</pmid><doi>10.1016/j.ceca.2005.06.020</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell calcium (Edinburgh), 2005-09, Vol.38 (3), p.417-425 |
| issn | 0143-4160 1532-1991 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals Apoptosis Apoptosis - physiology Calcium - physiology Calcium Channels - physiology Degeneration Excitotoxicity Homeostasis - physiology Humans Isquemia Mitochondria Neuroglia - physiology Reactive oxygen species |
| title | Calcium and glial cell death |
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