EAAC1 glutamate transporter expression in the rat lithium-pilocarpine model of temporal lobe epilepsy
Glutamate excitotoxicity has been involved in the pathophysiology of epilepsy. Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the n...
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| Veröffentlicht in: | Journal of cerebral blood flow and metabolism 2006-11, Vol.26 (11), p.1419-1430 |
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| creator | Voutsinos-Porche, Brigitte Koning, Estelle Cléent, Yann Kaplan, Hervé Ferrandon, Arielle Motte, Jacques Nehlig, Astrid |
| description | Glutamate excitotoxicity has been involved in the pathophysiology of epilepsy. Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the neuronal glutamate transporter (EAAC1) in the lithium-pilocarpine rat model of temporal lobe epilepsy. During the acute period of lithium-pilocarpine-induced status epilepticus, EAAC1 transporter expression increased in the pyramidal neurons of cornus ammonis (CA)1, CA2 and CA3 (fields of the hippocampus), in dentate gyrus (DG) granule cells and in olfactory tubercle (Tu). During the latent period, EAAC1 expression was strongly expressed in the DG granular and molecular layers, Tu, cerebral cortex and septum, and went back to control levels in CA1, CA2 and CA3 layers. The overexpression of EAAC1 occurred mainly in structures prone to develop Fluoro-Jade-B-positive degenerating neurons. It is, however, not clear to what extent the overexpression of EAAC1 contributes to epileptogenesis and in which area it may represent a preventive or compensatory or response to injury. |
| doi_str_mv | 10.1038/sj.jcbfm.9600295 |
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Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the neuronal glutamate transporter (EAAC1) in the lithium-pilocarpine rat model of temporal lobe epilepsy. During the acute period of lithium-pilocarpine-induced status epilepticus, EAAC1 transporter expression increased in the pyramidal neurons of cornus ammonis (CA)1, CA2 and CA3 (fields of the hippocampus), in dentate gyrus (DG) granule cells and in olfactory tubercle (Tu). During the latent period, EAAC1 expression was strongly expressed in the DG granular and molecular layers, Tu, cerebral cortex and septum, and went back to control levels in CA1, CA2 and CA3 layers. The overexpression of EAAC1 occurred mainly in structures prone to develop Fluoro-Jade-B-positive degenerating neurons. It is, however, not clear to what extent the overexpression of EAAC1 contributes to epileptogenesis and in which area it may represent a preventive or compensatory or response to injury.</description><identifier>ISSN: 0271-678X</identifier><identifier>EISSN: 1559-7016</identifier><identifier>DOI: 10.1038/sj.jcbfm.9600295</identifier><identifier>PMID: 16538232</identifier><identifier>CODEN: JCBMDN</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Animals ; Biological and medical sciences ; Brain - pathology ; Brain Chemistry - drug effects ; Brain Chemistry - physiology ; Epilepsy, Temporal Lobe - chemically induced ; Epilepsy, Temporal Lobe - metabolism ; Epilepsy, Temporal Lobe - pathology ; Excitatory Amino Acid Transporter 3 - biosynthesis ; Fluoresceins ; Immunohistochemistry ; Lithium Chloride ; Medical sciences ; Metabolic diseases ; Nerve Degeneration ; Neurology ; Neuropharmacology ; Neuroprotective agent ; Organic Chemicals ; Other metabolic disorders ; Pharmacology. Drug treatments ; Pigments (porphyrias, hyperbilirubinemias...) ; Pilocarpine ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus - chemically induced ; Status Epilepticus - physiopathology ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Journal of cerebral blood flow and metabolism, 2006-11, Vol.26 (11), p.1419-1430</ispartof><rights>2006 ISCBFM</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Nov 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c512t-a6041f47eacc9e2d650cfee03ec3067c5bcf13383dc4013ea5fbd81692c9d8543</citedby><cites>FETCH-LOGICAL-c512t-a6041f47eacc9e2d650cfee03ec3067c5bcf13383dc4013ea5fbd81692c9d8543</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://journals.sagepub.com/doi/pdf/10.1038/sj.jcbfm.9600295$$EPDF$$P50$$Gsage$$H</linktopdf><linktohtml>$$Uhttps://journals.sagepub.com/doi/10.1038/sj.jcbfm.9600295$$EHTML$$P50$$Gsage$$H</linktohtml><link.rule.ids>314,780,784,21819,27924,27925,43621,43622</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18674487$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16538232$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Voutsinos-Porche, Brigitte</creatorcontrib><creatorcontrib>Koning, Estelle</creatorcontrib><creatorcontrib>Cléent, Yann</creatorcontrib><creatorcontrib>Kaplan, Hervé</creatorcontrib><creatorcontrib>Ferrandon, Arielle</creatorcontrib><creatorcontrib>Motte, Jacques</creatorcontrib><creatorcontrib>Nehlig, Astrid</creatorcontrib><title>EAAC1 glutamate transporter expression in the rat lithium-pilocarpine model of temporal lobe epilepsy</title><title>Journal of cerebral blood flow and metabolism</title><addtitle>J Cereb Blood Flow Metab</addtitle><description>Glutamate excitotoxicity has been involved in the pathophysiology of epilepsy. Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the neuronal glutamate transporter (EAAC1) in the lithium-pilocarpine rat model of temporal lobe epilepsy. During the acute period of lithium-pilocarpine-induced status epilepticus, EAAC1 transporter expression increased in the pyramidal neurons of cornus ammonis (CA)1, CA2 and CA3 (fields of the hippocampus), in dentate gyrus (DG) granule cells and in olfactory tubercle (Tu). During the latent period, EAAC1 expression was strongly expressed in the DG granular and molecular layers, Tu, cerebral cortex and septum, and went back to control levels in CA1, CA2 and CA3 layers. The overexpression of EAAC1 occurred mainly in structures prone to develop Fluoro-Jade-B-positive degenerating neurons. It is, however, not clear to what extent the overexpression of EAAC1 contributes to epileptogenesis and in which area it may represent a preventive or compensatory or response to injury.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>Brain Chemistry - drug effects</subject><subject>Brain Chemistry - physiology</subject><subject>Epilepsy, Temporal Lobe - chemically induced</subject><subject>Epilepsy, Temporal Lobe - metabolism</subject><subject>Epilepsy, Temporal Lobe - pathology</subject><subject>Excitatory Amino Acid Transporter 3 - biosynthesis</subject><subject>Fluoresceins</subject><subject>Immunohistochemistry</subject><subject>Lithium Chloride</subject><subject>Medical sciences</subject><subject>Metabolic diseases</subject><subject>Nerve Degeneration</subject><subject>Neurology</subject><subject>Neuropharmacology</subject><subject>Neuroprotective agent</subject><subject>Organic Chemicals</subject><subject>Other metabolic disorders</subject><subject>Pharmacology. Drug treatments</subject><subject>Pigments (porphyrias, hyperbilirubinemias...)</subject><subject>Pilocarpine</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Status Epilepticus - chemically induced</subject><subject>Status Epilepticus - physiopathology</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0271-678X</issn><issn>1559-7016</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</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><sourceid>GNUQQ</sourceid><recordid>eNp9kc2L1TAUxYMoznN070YJgrjqMx_NR5ePxzgjDLhRcBfS9GamJW1qkoLz39vxVR-4cHUX93fOvZyD0GtK9pRw_TEP-8G1ftw3khDWiCdoR4VoKkWofIp2hClaSaW_X6AXOQ-EEM2FeI4uqBRcM852CK4OhyPFd2EpdrQFcEl2ynNMBRKGn3OCnPs44X7C5R5wsgWHvtz3y1jNfYjOprmfAI-xg4CjxwXGVWwDDrEFDCsDc354iZ55GzK82uYl-vbp6uvxprr9cv35eLitnKCsVFaSmvpagXWuAdZJQZwHIBwcJ1I50TpPOde8czWhHKzwbaepbJhrOi1qfok-nHznFH8skIsZ--wgBDtBXLLRSjKmFH0k3_1DDnFJ0_qcYbQRYk2nWSFyglyKOSfwZk79aNODocQ8FmDyYH4XYLYCVsnbzXdpR-jOgi3xFXi_ATY7G_wat-vzmdNS1bVWK1eduGzv4Pzcfw6_OfGTLUuCv4Z_9r8AQiOpgw</recordid><startdate>20061101</startdate><enddate>20061101</enddate><creator>Voutsinos-Porche, Brigitte</creator><creator>Koning, Estelle</creator><creator>Cléent, Yann</creator><creator>Kaplan, Hervé</creator><creator>Ferrandon, Arielle</creator><creator>Motte, Jacques</creator><creator>Nehlig, Astrid</creator><general>SAGE Publications</general><general>Lippincott Williams & Wilkins</general><general>Sage Publications Ltd</general><scope>IQODW</scope><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>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7TK</scope></search><sort><creationdate>20061101</creationdate><title>EAAC1 glutamate transporter expression in the rat lithium-pilocarpine model of temporal lobe epilepsy</title><author>Voutsinos-Porche, Brigitte ; Koning, Estelle ; Cléent, Yann ; Kaplan, Hervé ; Ferrandon, Arielle ; Motte, Jacques ; Nehlig, Astrid</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c512t-a6041f47eacc9e2d650cfee03ec3067c5bcf13383dc4013ea5fbd81692c9d8543</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>Brain Chemistry - drug effects</topic><topic>Brain Chemistry - physiology</topic><topic>Epilepsy, Temporal Lobe - chemically induced</topic><topic>Epilepsy, Temporal Lobe - metabolism</topic><topic>Epilepsy, Temporal Lobe - pathology</topic><topic>Excitatory Amino Acid Transporter 3 - biosynthesis</topic><topic>Fluoresceins</topic><topic>Immunohistochemistry</topic><topic>Lithium Chloride</topic><topic>Medical sciences</topic><topic>Metabolic diseases</topic><topic>Nerve Degeneration</topic><topic>Neurology</topic><topic>Neuropharmacology</topic><topic>Neuroprotective agent</topic><topic>Organic Chemicals</topic><topic>Other metabolic disorders</topic><topic>Pharmacology. Drug treatments</topic><topic>Pigments (porphyrias, hyperbilirubinemias...)</topic><topic>Pilocarpine</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Status Epilepticus - chemically induced</topic><topic>Status Epilepticus - physiopathology</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Voutsinos-Porche, Brigitte</creatorcontrib><creatorcontrib>Koning, Estelle</creatorcontrib><creatorcontrib>Cléent, Yann</creatorcontrib><creatorcontrib>Kaplan, Hervé</creatorcontrib><creatorcontrib>Ferrandon, Arielle</creatorcontrib><creatorcontrib>Motte, Jacques</creatorcontrib><creatorcontrib>Nehlig, Astrid</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Neurosciences Abstracts</collection><jtitle>Journal of cerebral blood flow and metabolism</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Voutsinos-Porche, Brigitte</au><au>Koning, Estelle</au><au>Cléent, Yann</au><au>Kaplan, Hervé</au><au>Ferrandon, Arielle</au><au>Motte, Jacques</au><au>Nehlig, Astrid</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EAAC1 glutamate transporter expression in the rat lithium-pilocarpine model of temporal lobe epilepsy</atitle><jtitle>Journal of cerebral blood flow and metabolism</jtitle><addtitle>J Cereb Blood Flow Metab</addtitle><date>2006-11-01</date><risdate>2006</risdate><volume>26</volume><issue>11</issue><spage>1419</spage><epage>1430</epage><pages>1419-1430</pages><issn>0271-678X</issn><eissn>1559-7016</eissn><coden>JCBMDN</coden><abstract>Glutamate excitotoxicity has been involved in the pathophysiology of epilepsy. Normal functioning of glutamate transporters clears the synaptically released glutamate to prevent excitotoxic neuronal death. Using densitometric immunohistochemical analysis, we examined the temporal expression of the neuronal glutamate transporter (EAAC1) in the lithium-pilocarpine rat model of temporal lobe epilepsy. During the acute period of lithium-pilocarpine-induced status epilepticus, EAAC1 transporter expression increased in the pyramidal neurons of cornus ammonis (CA)1, CA2 and CA3 (fields of the hippocampus), in dentate gyrus (DG) granule cells and in olfactory tubercle (Tu). During the latent period, EAAC1 expression was strongly expressed in the DG granular and molecular layers, Tu, cerebral cortex and septum, and went back to control levels in CA1, CA2 and CA3 layers. The overexpression of EAAC1 occurred mainly in structures prone to develop Fluoro-Jade-B-positive degenerating neurons. It is, however, not clear to what extent the overexpression of EAAC1 contributes to epileptogenesis and in which area it may represent a preventive or compensatory or response to injury.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>16538232</pmid><doi>10.1038/sj.jcbfm.9600295</doi><tpages>12</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Brain - pathology Brain Chemistry - drug effects Brain Chemistry - physiology Epilepsy, Temporal Lobe - chemically induced Epilepsy, Temporal Lobe - metabolism Epilepsy, Temporal Lobe - pathology Excitatory Amino Acid Transporter 3 - biosynthesis Fluoresceins Immunohistochemistry Lithium Chloride Medical sciences Metabolic diseases Nerve Degeneration Neurology Neuropharmacology Neuroprotective agent Organic Chemicals Other metabolic disorders Pharmacology. Drug treatments Pigments (porphyrias, hyperbilirubinemias...) Pilocarpine Rats Rats, Sprague-Dawley Status Epilepticus - chemically induced Status Epilepticus - physiopathology Vascular diseases and vascular malformations of the nervous system |
| title | EAAC1 glutamate transporter expression in the rat lithium-pilocarpine model of temporal lobe epilepsy |
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