Compensatory change in EAAC1 glutamate transporter in rat hippocampus CA1 region during kindling epileptogenesis
Functional and molecular changes in glutamate transporters during kindling epileptogenesis were investigated in hippocampus CA1-region of rats. In control animals total glutamate transporter activity was indicated by the stimulatory effect of the high-affinity transporter blocker l- trans-pyrrolidin...
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| Veröffentlicht in: | Neuroscience letters 1999-12, Vol.276 (3), p.157-160 |
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| creator | Ghijsen, W.E.J.M da Silva Aresta Belo, A.I Zuiderwijk, M Lopes da Silva, F.H |
| description | Functional and molecular changes in glutamate transporters during kindling epileptogenesis were investigated in hippocampus CA1-region of rats. In control animals total glutamate transporter activity was indicated by the stimulatory effect of the high-affinity transporter blocker
l-
trans-pyrrolidine-2,4-dicarboxylate on extracellular glutamate and aspartate concentrations, as measured by in vivo microdialysis. This blocker-induced elevation was absent already early during epileptogenesis. CA1 levels of the glutamate transporter subtypes GLAST and GLT-1, analyzed by quantitative immunoblotting, did not change during kindling epileptogenesis. However, the 60% decrease in EAAC-1 level observed in age-matched controls was fully compensated for in kindled animals 4–5 weeks after the last generalized seizure. These results indicate a compensatory change of the neuronal EAAC-1 glutamate transporter in CA1 region during kindling epileptogenesis, which may be the consequence of a decrease in total transporter activity. |
| doi_str_mv | 10.1016/S0304-3940(99)00824-1 |
| format | Article |
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l-
trans-pyrrolidine-2,4-dicarboxylate on extracellular glutamate and aspartate concentrations, as measured by in vivo microdialysis. This blocker-induced elevation was absent already early during epileptogenesis. CA1 levels of the glutamate transporter subtypes GLAST and GLT-1, analyzed by quantitative immunoblotting, did not change during kindling epileptogenesis. However, the 60% decrease in EAAC-1 level observed in age-matched controls was fully compensated for in kindled animals 4–5 weeks after the last generalized seizure. These results indicate a compensatory change of the neuronal EAAC-1 glutamate transporter in CA1 region during kindling epileptogenesis, which may be the consequence of a decrease in total transporter activity.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/S0304-3940(99)00824-1</identifier><identifier>PMID: 10612629</identifier><identifier>CODEN: NELED5</identifier><language>eng</language><publisher>Shannon: Elsevier Ireland Ltd</publisher><subject>Adaptation, Physiological ; Amino Acid Transport System X-AG ; Animals ; Aspartate ; Aspartic Acid - metabolism ; ATP-Binding Cassette Transporters - metabolism ; Biological and medical sciences ; CA1-region ; Carrier Proteins - metabolism ; Dicarboxylic Acids - pharmacology ; Epilepsy ; Epilepsy - etiology ; Excitatory Amino Acid Transporter 1 ; Excitatory Amino Acid Transporter 3 ; Extracellular Space - metabolism ; Glutamate ; Glutamate Plasma Membrane Transport Proteins ; Glutamic Acid - metabolism ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Hippocampus ; Hippocampus - metabolism ; Immunoblotting ; In vivo ; Kindling, Neurologic ; Medical sciences ; Microdialysis ; Nervous system (semeiology, syndromes) ; Neurology ; Pyrrolidines - pharmacology ; Rats ; Rats, Wistar ; Symporters ; Transporter</subject><ispartof>Neuroscience letters, 1999-12, Vol.276 (3), p.157-160</ispartof><rights>1999 Elsevier Science Ireland Ltd</rights><rights>2000 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c421t-187c1ee3c3afc3eb8df110f2e175c8859767f2dec82752a248a258f0c3ff964e3</citedby><cites>FETCH-LOGICAL-c421t-187c1ee3c3afc3eb8df110f2e175c8859767f2dec82752a248a258f0c3ff964e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304394099008241$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1192366$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10612629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ghijsen, W.E.J.M</creatorcontrib><creatorcontrib>da Silva Aresta Belo, A.I</creatorcontrib><creatorcontrib>Zuiderwijk, M</creatorcontrib><creatorcontrib>Lopes da Silva, F.H</creatorcontrib><title>Compensatory change in EAAC1 glutamate transporter in rat hippocampus CA1 region during kindling epileptogenesis</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>Functional and molecular changes in glutamate transporters during kindling epileptogenesis were investigated in hippocampus CA1-region of rats. In control animals total glutamate transporter activity was indicated by the stimulatory effect of the high-affinity transporter blocker
l-
trans-pyrrolidine-2,4-dicarboxylate on extracellular glutamate and aspartate concentrations, as measured by in vivo microdialysis. This blocker-induced elevation was absent already early during epileptogenesis. CA1 levels of the glutamate transporter subtypes GLAST and GLT-1, analyzed by quantitative immunoblotting, did not change during kindling epileptogenesis. However, the 60% decrease in EAAC-1 level observed in age-matched controls was fully compensated for in kindled animals 4–5 weeks after the last generalized seizure. These results indicate a compensatory change of the neuronal EAAC-1 glutamate transporter in CA1 region during kindling epileptogenesis, which may be the consequence of a decrease in total transporter activity.</description><subject>Adaptation, Physiological</subject><subject>Amino Acid Transport System X-AG</subject><subject>Animals</subject><subject>Aspartate</subject><subject>Aspartic Acid - metabolism</subject><subject>ATP-Binding Cassette Transporters - metabolism</subject><subject>Biological and medical sciences</subject><subject>CA1-region</subject><subject>Carrier Proteins - metabolism</subject><subject>Dicarboxylic Acids - pharmacology</subject><subject>Epilepsy</subject><subject>Epilepsy - etiology</subject><subject>Excitatory Amino Acid Transporter 1</subject><subject>Excitatory Amino Acid Transporter 3</subject><subject>Extracellular Space - metabolism</subject><subject>Glutamate</subject><subject>Glutamate Plasma Membrane Transport Proteins</subject><subject>Glutamic Acid - metabolism</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Hippocampus</subject><subject>Hippocampus - metabolism</subject><subject>Immunoblotting</subject><subject>In vivo</subject><subject>Kindling, Neurologic</subject><subject>Medical sciences</subject><subject>Microdialysis</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Pyrrolidines - pharmacology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Symporters</subject><subject>Transporter</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1v1DAQhi0EokvhJ4B8QAgOAX_EcXxCq6gtSJU4AGfLdcapIbGN7SD135PtroBbTzPSPPP1vgi9pOQ9JbT78JVw0jZcteStUu8I6Vnb0EdoR3vJGqkke4x2f5Ez9KyUH4QQQUX7FJ1R0lHWMbVDaYhLglBMjfkO21sTJsA-4Iv9fqB4mtdqFlMB12xCSTFXyIdyNhXf-pSiNUtaCx72FGeYfAx4XLMPE_7pwzgfEkh-hlTjBAGKL8_RE2fmAi9O8Rx9v7z4Nnxqrr9cfR72141tGa3N9oalANxy4yyHm350lBLHgEph-14o2UnHRrA9k4IZ1vaGid4Ry51TXQv8HL05zk05_lqhVL34YmGeTYC4Ft0pLqXsyIMgla3gXIoNFEfQ5lhKBqdT9ovJd5oSffBE33uiD4JrpfS9J5pufa9OC9abBcb_uo4mbMDrE2CKNbPbpLa-_OOoYrzrNuzjEYNNtt8esi7WQ7Aw-gy26jH6By75A8rLqVw</recordid><startdate>19991210</startdate><enddate>19991210</enddate><creator>Ghijsen, W.E.J.M</creator><creator>da Silva Aresta Belo, A.I</creator><creator>Zuiderwijk, M</creator><creator>Lopes da Silva, F.H</creator><general>Elsevier Ireland Ltd</general><general>Elsevier</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>19991210</creationdate><title>Compensatory change in EAAC1 glutamate transporter in rat hippocampus CA1 region during kindling epileptogenesis</title><author>Ghijsen, W.E.J.M ; da Silva Aresta Belo, A.I ; Zuiderwijk, M ; Lopes da Silva, F.H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c421t-187c1ee3c3afc3eb8df110f2e175c8859767f2dec82752a248a258f0c3ff964e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Adaptation, Physiological</topic><topic>Amino Acid Transport System X-AG</topic><topic>Animals</topic><topic>Aspartate</topic><topic>Aspartic Acid - metabolism</topic><topic>ATP-Binding Cassette Transporters - metabolism</topic><topic>Biological and medical sciences</topic><topic>CA1-region</topic><topic>Carrier Proteins - metabolism</topic><topic>Dicarboxylic Acids - pharmacology</topic><topic>Epilepsy</topic><topic>Epilepsy - etiology</topic><topic>Excitatory Amino Acid Transporter 1</topic><topic>Excitatory Amino Acid Transporter 3</topic><topic>Extracellular Space - metabolism</topic><topic>Glutamate</topic><topic>Glutamate Plasma Membrane Transport Proteins</topic><topic>Glutamic Acid - metabolism</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Hippocampus</topic><topic>Hippocampus - metabolism</topic><topic>Immunoblotting</topic><topic>In vivo</topic><topic>Kindling, Neurologic</topic><topic>Medical sciences</topic><topic>Microdialysis</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Pyrrolidines - pharmacology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Symporters</topic><topic>Transporter</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ghijsen, W.E.J.M</creatorcontrib><creatorcontrib>da Silva Aresta Belo, A.I</creatorcontrib><creatorcontrib>Zuiderwijk, M</creatorcontrib><creatorcontrib>Lopes da Silva, F.H</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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ghijsen, W.E.J.M</au><au>da Silva Aresta Belo, A.I</au><au>Zuiderwijk, M</au><au>Lopes da Silva, F.H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Compensatory change in EAAC1 glutamate transporter in rat hippocampus CA1 region during kindling epileptogenesis</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>1999-12-10</date><risdate>1999</risdate><volume>276</volume><issue>3</issue><spage>157</spage><epage>160</epage><pages>157-160</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><coden>NELED5</coden><abstract>Functional and molecular changes in glutamate transporters during kindling epileptogenesis were investigated in hippocampus CA1-region of rats. In control animals total glutamate transporter activity was indicated by the stimulatory effect of the high-affinity transporter blocker
l-
trans-pyrrolidine-2,4-dicarboxylate on extracellular glutamate and aspartate concentrations, as measured by in vivo microdialysis. This blocker-induced elevation was absent already early during epileptogenesis. CA1 levels of the glutamate transporter subtypes GLAST and GLT-1, analyzed by quantitative immunoblotting, did not change during kindling epileptogenesis. However, the 60% decrease in EAAC-1 level observed in age-matched controls was fully compensated for in kindled animals 4–5 weeks after the last generalized seizure. These results indicate a compensatory change of the neuronal EAAC-1 glutamate transporter in CA1 region during kindling epileptogenesis, which may be the consequence of a decrease in total transporter activity.</abstract><cop>Shannon</cop><pub>Elsevier Ireland Ltd</pub><pmid>10612629</pmid><doi>10.1016/S0304-3940(99)00824-1</doi><tpages>4</tpages></addata></record> |
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| ispartof | Neuroscience letters, 1999-12, Vol.276 (3), p.157-160 |
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| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Adaptation, Physiological Amino Acid Transport System X-AG Animals Aspartate Aspartic Acid - metabolism ATP-Binding Cassette Transporters - metabolism Biological and medical sciences CA1-region Carrier Proteins - metabolism Dicarboxylic Acids - pharmacology Epilepsy Epilepsy - etiology Excitatory Amino Acid Transporter 1 Excitatory Amino Acid Transporter 3 Extracellular Space - metabolism Glutamate Glutamate Plasma Membrane Transport Proteins Glutamic Acid - metabolism Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Hippocampus Hippocampus - metabolism Immunoblotting In vivo Kindling, Neurologic Medical sciences Microdialysis Nervous system (semeiology, syndromes) Neurology Pyrrolidines - pharmacology Rats Rats, Wistar Symporters Transporter |
| title | Compensatory change in EAAC1 glutamate transporter in rat hippocampus CA1 region during kindling epileptogenesis |
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