The Expression of Kainate Receptor Subunits in Hippocampal Astrocytes After Experimentally Induced Status Epilepticus
ABSTRACTAstrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)–positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under ba...
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description | ABSTRACTAstrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)–positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy, we show by immunohistochemistry and colocalization analysis that reactive hippocampal astrocytes express kainate receptor (KAR) subunits after SE. In the CA1 region, GluK1, GluK2/3, GluK4, and GluK5 subunit expression was observed in GFAP-positive astrocytes during the seizure-free or “latent” period 1 week after SE. At 8 weeks after SE, a time after SE when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits remained expressed at significant levels. Kainate receptor subunit expression was found in astrocytes in the hippocampus and surrounding cortex but not in GFAP-positive astrocytes of striatum, olfactory bulb, or brainstem. To examine hippocampal KAR expression more broadly, astroglial-enriched tissue fractions were prepared from dissected hippocampi and were found to have greater GluK4 expression after SE than controls. These results demonstrate that astrocytes begin to express KARs after seizure activity and suggest that their expression may contribute to the pathophysiology of epilepsy. |
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Koji ; Thomson, Kyle E. ; Wilcox, Karen S.</creator><creatorcontrib>Vargas, Jay R. ; Takahashi, D. Koji ; Thomson, Kyle E. ; Wilcox, Karen S.</creatorcontrib><description>ABSTRACTAstrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)–positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy, we show by immunohistochemistry and colocalization analysis that reactive hippocampal astrocytes express kainate receptor (KAR) subunits after SE. In the CA1 region, GluK1, GluK2/3, GluK4, and GluK5 subunit expression was observed in GFAP-positive astrocytes during the seizure-free or “latent” period 1 week after SE. At 8 weeks after SE, a time after SE when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits remained expressed at significant levels. Kainate receptor subunit expression was found in astrocytes in the hippocampus and surrounding cortex but not in GFAP-positive astrocytes of striatum, olfactory bulb, or brainstem. To examine hippocampal KAR expression more broadly, astroglial-enriched tissue fractions were prepared from dissected hippocampi and were found to have greater GluK4 expression after SE than controls. These results demonstrate that astrocytes begin to express KARs after seizure activity and suggest that their expression may contribute to the pathophysiology of epilepsy.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/NEN.0b013e3182a4b266</identifier><identifier>PMID: 24042195</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>England: by American Association of Neuropathologists, Inc</publisher><subject>Animals ; Astrocytes - metabolism ; Behavior ; Epilepsy ; Glial Fibrillary Acidic Protein - metabolism ; Gliosis - genetics ; Gliosis - metabolism ; Hippocampus - metabolism ; Kainic Acid ; Laboratory animals ; Male ; Neurons - metabolism ; Pilocarpine ; Protein Subunits - metabolism ; Proteins ; Rats ; Rats, Sprague-Dawley ; Receptors, Kainic Acid - metabolism ; Rodents ; Seizures - metabolism ; Status Epilepticus - chemically induced ; Status Epilepticus - metabolism</subject><ispartof>Journal of neuropathology and experimental neurology, 2013-10, Vol.72 (10), p.919-932</ispartof><rights>2013 by American Association of Neuropathologists, Inc.</rights><rights>Copyright Lippincott Williams & Wilkins Oct 2013</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5806-53c0d34d098e7b92d02e3082c25c8ac41bbec6293a13a0a06bd1b33b34be8bfe3</citedby><cites>FETCH-LOGICAL-c5806-53c0d34d098e7b92d02e3082c25c8ac41bbec6293a13a0a06bd1b33b34be8bfe3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24042195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Vargas, Jay R.</creatorcontrib><creatorcontrib>Takahashi, D. Koji</creatorcontrib><creatorcontrib>Thomson, Kyle E.</creatorcontrib><creatorcontrib>Wilcox, Karen S.</creatorcontrib><title>The Expression of Kainate Receptor Subunits in Hippocampal Astrocytes After Experimentally Induced Status Epilepticus</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>ABSTRACTAstrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)–positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy, we show by immunohistochemistry and colocalization analysis that reactive hippocampal astrocytes express kainate receptor (KAR) subunits after SE. In the CA1 region, GluK1, GluK2/3, GluK4, and GluK5 subunit expression was observed in GFAP-positive astrocytes during the seizure-free or “latent” period 1 week after SE. At 8 weeks after SE, a time after SE when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits remained expressed at significant levels. Kainate receptor subunit expression was found in astrocytes in the hippocampus and surrounding cortex but not in GFAP-positive astrocytes of striatum, olfactory bulb, or brainstem. To examine hippocampal KAR expression more broadly, astroglial-enriched tissue fractions were prepared from dissected hippocampi and were found to have greater GluK4 expression after SE than controls. These results demonstrate that astrocytes begin to express KARs after seizure activity and suggest that their expression may contribute to the pathophysiology of epilepsy.</description><subject>Animals</subject><subject>Astrocytes - metabolism</subject><subject>Behavior</subject><subject>Epilepsy</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Gliosis - genetics</subject><subject>Gliosis - metabolism</subject><subject>Hippocampus - metabolism</subject><subject>Kainic Acid</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Neurons - metabolism</subject><subject>Pilocarpine</subject><subject>Protein Subunits - metabolism</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Kainic Acid - metabolism</subject><subject>Rodents</subject><subject>Seizures - metabolism</subject><subject>Status Epilepticus - chemically induced</subject><subject>Status Epilepticus - metabolism</subject><issn>0022-3069</issn><issn>1554-6578</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><sourceid>GNUQQ</sourceid><recordid>eNp9kU1P3DAQhq2qFSyUf1BVlnrhEjr-yjrHFVoKKqJSoefIdibaUG-c-kOw_75ZLeXAoae5PO-jmXkJ-cTggkGz_Hq3vrsAC0ygYJobaXldvyMLppSsarXU78kCgPNKQN0ck5OUHgGggUYekWMuQXLWqAUpDxuk6-cpYkpDGGno6XczjCYj_YkOpxwivS-2jENOdBjp9TBNwZntZDxdpRyD22VMdNVnjHsPxmGLYzbe7-jN2BWHHb3PJpdE19PgZ-HgSvpIPvTGJzx7mafk19X64fK6uv3x7eZydVs5paGulHDQCdlBo3FpG94BRwGaO66cNk4ya9HVvBGGCQMGatsxK4QV0qK2PYpTcn7wTjH8KZhyux2SQ-_NiKGklkmllWBLzmb0yxv0MZQ4ztvNlORaaVHvKXmgXAwpRezbaT7YxF3LoN3X0s61tG9rmWOfX-TFbrF7Df3rYQb0AXgKfv5k-u3LE8Z2g8bnzf_dfwGFkJzX</recordid><startdate>201310</startdate><enddate>201310</enddate><creator>Vargas, Jay R.</creator><creator>Takahashi, D. 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Koji ; Thomson, Kyle E. ; Wilcox, Karen S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5806-53c0d34d098e7b92d02e3082c25c8ac41bbec6293a13a0a06bd1b33b34be8bfe3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Astrocytes - metabolism</topic><topic>Behavior</topic><topic>Epilepsy</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Gliosis - genetics</topic><topic>Gliosis - metabolism</topic><topic>Hippocampus - metabolism</topic><topic>Kainic Acid</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Neurons - metabolism</topic><topic>Pilocarpine</topic><topic>Protein Subunits - metabolism</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Kainic Acid - metabolism</topic><topic>Rodents</topic><topic>Seizures - metabolism</topic><topic>Status Epilepticus - chemically induced</topic><topic>Status Epilepticus - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Vargas, Jay R.</creatorcontrib><creatorcontrib>Takahashi, D. 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Koji</au><au>Thomson, Kyle E.</au><au>Wilcox, Karen S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Expression of Kainate Receptor Subunits in Hippocampal Astrocytes After Experimentally Induced Status Epilepticus</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>2013-10</date><risdate>2013</risdate><volume>72</volume><issue>10</issue><spage>919</spage><epage>932</epage><pages>919-932</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><abstract>ABSTRACTAstrocytes have emerged as active participants of synaptic transmission and are increasingly implicated in neurologic disorders including epilepsy. Adult glial fibrillary acidic protein (GFAP)–positive hippocampal astrocytes are not known for ionotropic glutamate receptor expression under basal conditions. Using a chemoconvulsive status epilepticus (SE) model of temporal lobe epilepsy, we show by immunohistochemistry and colocalization analysis that reactive hippocampal astrocytes express kainate receptor (KAR) subunits after SE. In the CA1 region, GluK1, GluK2/3, GluK4, and GluK5 subunit expression was observed in GFAP-positive astrocytes during the seizure-free or “latent” period 1 week after SE. At 8 weeks after SE, a time after SE when spontaneous behavioral seizures occur, the GluK1 and GluK5 subunits remained expressed at significant levels. Kainate receptor subunit expression was found in astrocytes in the hippocampus and surrounding cortex but not in GFAP-positive astrocytes of striatum, olfactory bulb, or brainstem. To examine hippocampal KAR expression more broadly, astroglial-enriched tissue fractions were prepared from dissected hippocampi and were found to have greater GluK4 expression after SE than controls. These results demonstrate that astrocytes begin to express KARs after seizure activity and suggest that their expression may contribute to the pathophysiology of epilepsy.</abstract><cop>England</cop><pub>by American Association of Neuropathologists, Inc</pub><pmid>24042195</pmid><doi>10.1097/NEN.0b013e3182a4b266</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Astrocytes - metabolism Behavior Epilepsy Glial Fibrillary Acidic Protein - metabolism Gliosis - genetics Gliosis - metabolism Hippocampus - metabolism Kainic Acid Laboratory animals Male Neurons - metabolism Pilocarpine Protein Subunits - metabolism Proteins Rats Rats, Sprague-Dawley Receptors, Kainic Acid - metabolism Rodents Seizures - metabolism Status Epilepticus - chemically induced Status Epilepticus - metabolism |
title | The Expression of Kainate Receptor Subunits in Hippocampal Astrocytes After Experimentally Induced Status Epilepticus |
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