Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus
In the present study we analyzed aquaporin‐4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine‐induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non‐SE‐induced animals, AQP4 immunoreactivity was diffuse...
Gespeichert in:
| Veröffentlicht in: | Journal of comparative neurology (1911) 2010-11, Vol.518 (22), p.4612-4628 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 4628 |
|---|---|
| container_issue | 22 |
| container_start_page | 4612 |
| container_title | Journal of comparative neurology (1911) |
| container_volume | 518 |
| creator | Kim, Ji-Eun Yeo, Seong-Il Ryu, Hea Jin Kim, Min-Ju Kim, Duk-Soo Jo, Seung-Mook Kang, Tae-Cheon |
| description | In the present study we analyzed aquaporin‐4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine‐induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non‐SE‐induced animals, AQP4 immunoreactivity was diffusely detected in the PC and the hippocampus. AQP4 immunoreactivity was mainly observed in the endfeet of astrocytes. Following SE the AQP4‐deleted area was clearly detected in the PC, not in the hippocampus. Decreases in dystrophin and α‐syntrophin immunoreactivities were followed by reduction in AQP4 immunoreactivity. These alterations were accompanied by the development of vasogenic edema and the astroglial loss in the PC. In addition, acetazolamide (an AQP4 inhibitor) treatment exacerbated vasogenic edema and astroglial loss both in the PC and in the hippocampus. These findings suggest that SE may induce impairments of astroglial AQP4 functions via disruption of the dystrophin/α‐syntrophin complex that worsen vasogenic edema. Subsequently, vasogenic edema results in extensive astroglial loss that may aggravate vasogenic edema. J. Comp. Neurol. 518:4612–4628, 2010. © 2010 Wiley‐Liss, Inc. |
| doi_str_mv | 10.1002/cne.22482 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_883031063</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3958024001</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4542-bf5647a87fb7bc570f52eb295bc1057af574d158d89b6663dcaa27e9e4d19f103</originalsourceid><addsrcrecordid>eNqFkU1LHTEUhkOp1Kvton-gBLooXYzmY_K11IvagthNi-5CJpPR2MxkmmSwrvrXjV51URBXgXOe94WcB4CPGO1hhMi-ndweIa0kb8AKI8UbJTl-C1Z1hxuluNgGOzlfI4SUovId2CZISs4JW4F_B7mkeBm8CTDEnKGZeuh6Nxo4xDSa4uME_QTLlYPJFDj75O8X0MZU3N8H_MrPc7RmnJdcQyHEGz9dVjLUYZr95Bo_9Yt1PczFlAq5unNz8XbJ78HWYEJ2Hx7fXfDr-Ojn-ltz-uPk-_rgtLEta0nTDYy3wkgxdKKzTKCBEdcRxTqLERNmYKLtMZO9VB3nnPbWGCKccnWqBozoLviy6Z1T_LO4XPTos3UhmMnFJWspKaIYcfo6KVQr6u1eJwXjnCksVSU__0dexyVN9cMaC84lplyJSn3dUDZVE8kNek5-NOlWY6TvResqWj-Iruynx8alG13_TD6ZrcD-Bript759uUmvz46eKptNwudq9jlh0m_NBRVMn5-daHl4TA-RuNCI3gG1WMJe</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1766813697</pqid></control><display><type>article</type><title>Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus</title><source>MEDLINE</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Kim, Ji-Eun ; Yeo, Seong-Il ; Ryu, Hea Jin ; Kim, Min-Ju ; Kim, Duk-Soo ; Jo, Seung-Mook ; Kang, Tae-Cheon</creator><creatorcontrib>Kim, Ji-Eun ; Yeo, Seong-Il ; Ryu, Hea Jin ; Kim, Min-Ju ; Kim, Duk-Soo ; Jo, Seung-Mook ; Kang, Tae-Cheon</creatorcontrib><description>In the present study we analyzed aquaporin‐4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine‐induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non‐SE‐induced animals, AQP4 immunoreactivity was diffusely detected in the PC and the hippocampus. AQP4 immunoreactivity was mainly observed in the endfeet of astrocytes. Following SE the AQP4‐deleted area was clearly detected in the PC, not in the hippocampus. Decreases in dystrophin and α‐syntrophin immunoreactivities were followed by reduction in AQP4 immunoreactivity. These alterations were accompanied by the development of vasogenic edema and the astroglial loss in the PC. In addition, acetazolamide (an AQP4 inhibitor) treatment exacerbated vasogenic edema and astroglial loss both in the PC and in the hippocampus. These findings suggest that SE may induce impairments of astroglial AQP4 functions via disruption of the dystrophin/α‐syntrophin complex that worsen vasogenic edema. Subsequently, vasogenic edema results in extensive astroglial loss that may aggravate vasogenic edema. J. Comp. Neurol. 518:4612–4628, 2010. © 2010 Wiley‐Liss, Inc.</description><identifier>ISSN: 0021-9967</identifier><identifier>ISSN: 1096-9861</identifier><identifier>EISSN: 1096-9861</identifier><identifier>DOI: 10.1002/cne.22482</identifier><identifier>PMID: 20886625</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>acetazolamide ; Animals ; Aquaporin 4 ; Aquaporin 4 - metabolism ; astrocyte ; Astrocytes ; Astrocytes - pathology ; Brain ; Brain Edema - etiology ; Calcium-Binding Proteins - metabolism ; Cell Count - methods ; Cerebral Cortex - pathology ; Cerebral Cortex - physiopathology ; Cortex (piriform) ; Disease Models, Animal ; Dystrophin ; Dystrophin - metabolism ; Edema ; Epilepsy ; Gene Expression Regulation - drug effects ; Gene Expression Regulation - physiology ; Glial Fibrillary Acidic Protein - metabolism ; Hippocampus ; Hippocampus - pathology ; Hippocampus - physiopathology ; Immunoreactivity ; Lithium Chloride - toxicity ; Male ; Membrane Proteins - metabolism ; Muscle Proteins - metabolism ; Pilocarpine - toxicity ; piriform cortex ; Rats ; Rats, Sprague-Dawley ; Status Epilepticus - chemically induced ; Status Epilepticus - complications ; Status Epilepticus - pathology ; α-syntrophin</subject><ispartof>Journal of comparative neurology (1911), 2010-11, Vol.518 (22), p.4612-4628</ispartof><rights>Copyright © 2010 Wiley‐Liss, Inc.</rights><rights>Copyright © 2010 Wiley-Liss, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4542-bf5647a87fb7bc570f52eb295bc1057af574d158d89b6663dcaa27e9e4d19f103</citedby><cites>FETCH-LOGICAL-c4542-bf5647a87fb7bc570f52eb295bc1057af574d158d89b6663dcaa27e9e4d19f103</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fcne.22482$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fcne.22482$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20886625$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kim, Ji-Eun</creatorcontrib><creatorcontrib>Yeo, Seong-Il</creatorcontrib><creatorcontrib>Ryu, Hea Jin</creatorcontrib><creatorcontrib>Kim, Min-Ju</creatorcontrib><creatorcontrib>Kim, Duk-Soo</creatorcontrib><creatorcontrib>Jo, Seung-Mook</creatorcontrib><creatorcontrib>Kang, Tae-Cheon</creatorcontrib><title>Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus</title><title>Journal of comparative neurology (1911)</title><addtitle>J. Comp. Neurol</addtitle><description>In the present study we analyzed aquaporin‐4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine‐induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non‐SE‐induced animals, AQP4 immunoreactivity was diffusely detected in the PC and the hippocampus. AQP4 immunoreactivity was mainly observed in the endfeet of astrocytes. Following SE the AQP4‐deleted area was clearly detected in the PC, not in the hippocampus. Decreases in dystrophin and α‐syntrophin immunoreactivities were followed by reduction in AQP4 immunoreactivity. These alterations were accompanied by the development of vasogenic edema and the astroglial loss in the PC. In addition, acetazolamide (an AQP4 inhibitor) treatment exacerbated vasogenic edema and astroglial loss both in the PC and in the hippocampus. These findings suggest that SE may induce impairments of astroglial AQP4 functions via disruption of the dystrophin/α‐syntrophin complex that worsen vasogenic edema. Subsequently, vasogenic edema results in extensive astroglial loss that may aggravate vasogenic edema. J. Comp. Neurol. 518:4612–4628, 2010. © 2010 Wiley‐Liss, Inc.</description><subject>acetazolamide</subject><subject>Animals</subject><subject>Aquaporin 4</subject><subject>Aquaporin 4 - metabolism</subject><subject>astrocyte</subject><subject>Astrocytes</subject><subject>Astrocytes - pathology</subject><subject>Brain</subject><subject>Brain Edema - etiology</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Cell Count - methods</subject><subject>Cerebral Cortex - pathology</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Cortex (piriform)</subject><subject>Disease Models, Animal</subject><subject>Dystrophin</subject><subject>Dystrophin - metabolism</subject><subject>Edema</subject><subject>Epilepsy</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Gene Expression Regulation - physiology</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Hippocampus</subject><subject>Hippocampus - pathology</subject><subject>Hippocampus - physiopathology</subject><subject>Immunoreactivity</subject><subject>Lithium Chloride - toxicity</subject><subject>Male</subject><subject>Membrane Proteins - metabolism</subject><subject>Muscle Proteins - metabolism</subject><subject>Pilocarpine - toxicity</subject><subject>piriform cortex</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Status Epilepticus - chemically induced</subject><subject>Status Epilepticus - complications</subject><subject>Status Epilepticus - pathology</subject><subject>α-syntrophin</subject><issn>0021-9967</issn><issn>1096-9861</issn><issn>1096-9861</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1LHTEUhkOp1Kvton-gBLooXYzmY_K11IvagthNi-5CJpPR2MxkmmSwrvrXjV51URBXgXOe94WcB4CPGO1hhMi-ndweIa0kb8AKI8UbJTl-C1Z1hxuluNgGOzlfI4SUovId2CZISs4JW4F_B7mkeBm8CTDEnKGZeuh6Nxo4xDSa4uME_QTLlYPJFDj75O8X0MZU3N8H_MrPc7RmnJdcQyHEGz9dVjLUYZr95Bo_9Yt1PczFlAq5unNz8XbJ78HWYEJ2Hx7fXfDr-Ojn-ltz-uPk-_rgtLEta0nTDYy3wkgxdKKzTKCBEdcRxTqLERNmYKLtMZO9VB3nnPbWGCKccnWqBozoLviy6Z1T_LO4XPTos3UhmMnFJWspKaIYcfo6KVQr6u1eJwXjnCksVSU__0dexyVN9cMaC84lplyJSn3dUDZVE8kNek5-NOlWY6TvResqWj-Iruynx8alG13_TD6ZrcD-Bript759uUmvz46eKptNwudq9jlh0m_NBRVMn5-daHl4TA-RuNCI3gG1WMJe</recordid><startdate>20101115</startdate><enddate>20101115</enddate><creator>Kim, Ji-Eun</creator><creator>Yeo, Seong-Il</creator><creator>Ryu, Hea Jin</creator><creator>Kim, Min-Ju</creator><creator>Kim, Duk-Soo</creator><creator>Jo, Seung-Mook</creator><creator>Kang, Tae-Cheon</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7QR</scope><scope>7TK</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20101115</creationdate><title>Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus</title><author>Kim, Ji-Eun ; Yeo, Seong-Il ; Ryu, Hea Jin ; Kim, Min-Ju ; Kim, Duk-Soo ; Jo, Seung-Mook ; Kang, Tae-Cheon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4542-bf5647a87fb7bc570f52eb295bc1057af574d158d89b6663dcaa27e9e4d19f103</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>acetazolamide</topic><topic>Animals</topic><topic>Aquaporin 4</topic><topic>Aquaporin 4 - metabolism</topic><topic>astrocyte</topic><topic>Astrocytes</topic><topic>Astrocytes - pathology</topic><topic>Brain</topic><topic>Brain Edema - etiology</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Cell Count - methods</topic><topic>Cerebral Cortex - pathology</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Cortex (piriform)</topic><topic>Disease Models, Animal</topic><topic>Dystrophin</topic><topic>Dystrophin - metabolism</topic><topic>Edema</topic><topic>Epilepsy</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Gene Expression Regulation - physiology</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Hippocampus</topic><topic>Hippocampus - pathology</topic><topic>Hippocampus - physiopathology</topic><topic>Immunoreactivity</topic><topic>Lithium Chloride - toxicity</topic><topic>Male</topic><topic>Membrane Proteins - metabolism</topic><topic>Muscle Proteins - metabolism</topic><topic>Pilocarpine - toxicity</topic><topic>piriform cortex</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Status Epilepticus - chemically induced</topic><topic>Status Epilepticus - complications</topic><topic>Status Epilepticus - pathology</topic><topic>α-syntrophin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kim, Ji-Eun</creatorcontrib><creatorcontrib>Yeo, Seong-Il</creatorcontrib><creatorcontrib>Ryu, Hea Jin</creatorcontrib><creatorcontrib>Kim, Min-Ju</creatorcontrib><creatorcontrib>Kim, Duk-Soo</creatorcontrib><creatorcontrib>Jo, Seung-Mook</creatorcontrib><creatorcontrib>Kang, Tae-Cheon</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of comparative neurology (1911)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kim, Ji-Eun</au><au>Yeo, Seong-Il</au><au>Ryu, Hea Jin</au><au>Kim, Min-Ju</au><au>Kim, Duk-Soo</au><au>Jo, Seung-Mook</au><au>Kang, Tae-Cheon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus</atitle><jtitle>Journal of comparative neurology (1911)</jtitle><addtitle>J. Comp. Neurol</addtitle><date>2010-11-15</date><risdate>2010</risdate><volume>518</volume><issue>22</issue><spage>4612</spage><epage>4628</epage><pages>4612-4628</pages><issn>0021-9967</issn><issn>1096-9861</issn><eissn>1096-9861</eissn><abstract>In the present study we analyzed aquaporin‐4 (AQP4) immunoreactivity in the piriform cortex (PC) and the hippocampus of pilocarpine‐induced rat epilepsy model to elucidate the roles of AQP4 in brain edema following status epilepticus (SE). In non‐SE‐induced animals, AQP4 immunoreactivity was diffusely detected in the PC and the hippocampus. AQP4 immunoreactivity was mainly observed in the endfeet of astrocytes. Following SE the AQP4‐deleted area was clearly detected in the PC, not in the hippocampus. Decreases in dystrophin and α‐syntrophin immunoreactivities were followed by reduction in AQP4 immunoreactivity. These alterations were accompanied by the development of vasogenic edema and the astroglial loss in the PC. In addition, acetazolamide (an AQP4 inhibitor) treatment exacerbated vasogenic edema and astroglial loss both in the PC and in the hippocampus. These findings suggest that SE may induce impairments of astroglial AQP4 functions via disruption of the dystrophin/α‐syntrophin complex that worsen vasogenic edema. Subsequently, vasogenic edema results in extensive astroglial loss that may aggravate vasogenic edema. J. Comp. Neurol. 518:4612–4628, 2010. © 2010 Wiley‐Liss, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>20886625</pmid><doi>10.1002/cne.22482</doi><tpages>17</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0021-9967 |
| ispartof | Journal of comparative neurology (1911), 2010-11, Vol.518 (22), p.4612-4628 |
| issn | 0021-9967 1096-9861 1096-9861 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_883031063 |
| source | MEDLINE; Wiley Online Library Journals Frontfile Complete |
| subjects | acetazolamide Animals Aquaporin 4 Aquaporin 4 - metabolism astrocyte Astrocytes Astrocytes - pathology Brain Brain Edema - etiology Calcium-Binding Proteins - metabolism Cell Count - methods Cerebral Cortex - pathology Cerebral Cortex - physiopathology Cortex (piriform) Disease Models, Animal Dystrophin Dystrophin - metabolism Edema Epilepsy Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Glial Fibrillary Acidic Protein - metabolism Hippocampus Hippocampus - pathology Hippocampus - physiopathology Immunoreactivity Lithium Chloride - toxicity Male Membrane Proteins - metabolism Muscle Proteins - metabolism Pilocarpine - toxicity piriform cortex Rats Rats, Sprague-Dawley Status Epilepticus - chemically induced Status Epilepticus - complications Status Epilepticus - pathology α-syntrophin |
| title | Astroglial loss and edema formation in the rat piriform cortex and hippocampus following pilocarpine-induced status epilepticus |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-15T17%3A15%3A48IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Astroglial%20loss%20and%20edema%20formation%20in%20the%20rat%20piriform%20cortex%20and%20hippocampus%20following%20pilocarpine-induced%20status%20epilepticus&rft.jtitle=Journal%20of%20comparative%20neurology%20(1911)&rft.au=Kim,%20Ji-Eun&rft.date=2010-11-15&rft.volume=518&rft.issue=22&rft.spage=4612&rft.epage=4628&rft.pages=4612-4628&rft.issn=0021-9967&rft.eissn=1096-9861&rft_id=info:doi/10.1002/cne.22482&rft_dat=%3Cproquest_cross%3E3958024001%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1766813697&rft_id=info:pmid/20886625&rfr_iscdi=true |