Type II Glucocorticoid Receptors Are Involved in Neuronal Death and Astrocyte Activation Induced by Trimethyltin in the Rat Hippocampus
According to our previous study, trimethyltin (TMT), a neurotoxicant, induces the loss of pyramidal neurons in the rat hippocampus, which is preceded by a transient increase in plasma corticosterone concentration. To address whether this transient activation of the hypothalamopituitary–adrenocortica...
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| Veröffentlicht in: | Experimental neurology 2001-09, Vol.171 (1), p.22-28 |
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| creator | Imai, Hideki Nishimura, Tsutomu Sadamatsu, Miyuki Liu, Ying Kabuto, Michinori Kato, Nobumasa |
| description | According to our previous study, trimethyltin (TMT), a neurotoxicant, induces the loss of pyramidal neurons in the rat hippocampus, which is preceded by a transient increase in plasma corticosterone concentration. To address whether this transient activation of the hypothalamopituitary–adrenocortical axis is related to neuronal loss in the hippocampus, we evaluated the effects of bilateral adrenalectomy (ADX) and the chronic supplemental treatment of glucocorticoid receptor agonists after ADX on TMT-induced hippocampal damage. Peroral administration of a single dose of TMT (9 mg/kg body wt) induced the extensive loss of CA3 pyramidal neurons and reactive astrocytosis in the hippocampus, as evidenced by results of vimentin and glial fibrillary acidic protein immunohistochemistry, and the effects were profoundly exacerbated by bilateral adrenalectomy. Prolonged administration of corticosterone not only attenuated the exacerbating effects of adrenalectomy but also partially reversed the TMT-induced neuronal loss and reactive astrocytosis. Dexamethasone, but not aldosterone, could be substituted for corticosterone, suggesting a novel neuroprotective action of type II glucocorticoid receptors in the hippocampus. |
| doi_str_mv | 10.1006/exnr.2001.7725 |
| format | Article |
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To address whether this transient activation of the hypothalamopituitary–adrenocortical axis is related to neuronal loss in the hippocampus, we evaluated the effects of bilateral adrenalectomy (ADX) and the chronic supplemental treatment of glucocorticoid receptor agonists after ADX on TMT-induced hippocampal damage. Peroral administration of a single dose of TMT (9 mg/kg body wt) induced the extensive loss of CA3 pyramidal neurons and reactive astrocytosis in the hippocampus, as evidenced by results of vimentin and glial fibrillary acidic protein immunohistochemistry, and the effects were profoundly exacerbated by bilateral adrenalectomy. Prolonged administration of corticosterone not only attenuated the exacerbating effects of adrenalectomy but also partially reversed the TMT-induced neuronal loss and reactive astrocytosis. Dexamethasone, but not aldosterone, could be substituted for corticosterone, suggesting a novel neuroprotective action of type II glucocorticoid receptors in the hippocampus.</description><identifier>ISSN: 0014-4886</identifier><identifier>EISSN: 1090-2430</identifier><identifier>DOI: 10.1006/exnr.2001.7725</identifier><identifier>PMID: 11520118</identifier><identifier>CODEN: EXNEAC</identifier><language>eng</language><publisher>Amsterdam: Elsevier Inc</publisher><subject>Adrenalectomy ; aldosterone ; Aldosterone - pharmacology ; Animals ; Astrocytes - cytology ; Astrocytes - drug effects ; Astrocytes - metabolism ; Biological and medical sciences ; Blood. Blood coagulation. Reticuloendothelial system ; Cell Count ; Cell Death - drug effects ; dexamethasone ; Dexamethasone - pharmacology ; Glial Fibrillary Acidic Protein - biosynthesis ; Gliosis - chemically induced ; Gliosis - pathology ; Glucocorticoids - pharmacology ; hippocampus ; Hippocampus - cytology ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hypothalamo-Hypophyseal System - metabolism ; Immunohistochemistry ; Male ; Medical sciences ; Neurons - cytology ; Neurons - drug effects ; Neurons - metabolism ; Pharmacology. Drug treatments ; Pituitary-Adrenal System - metabolism ; Pyramidal Cells - cytology ; Pyramidal Cells - drug effects ; Pyramidal Cells - metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Glucocorticoid - agonists ; Receptors, Glucocorticoid - metabolism ; trimethyltin ; Trimethyltin Compounds - pharmacology ; vimentin ; Vimentin - biosynthesis</subject><ispartof>Experimental neurology, 2001-09, Vol.171 (1), p.22-28</ispartof><rights>2001 Academic Press</rights><rights>2002 INIST-CNRS</rights><rights>Copyright 2001 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-d7fdefbe94c3f8148d64ceef68f10c2f9a680a0c08e213cb244665dea95324573</citedby><cites>FETCH-LOGICAL-c436t-d7fdefbe94c3f8148d64ceef68f10c2f9a680a0c08e213cb244665dea95324573</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1006/exnr.2001.7725$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14058709$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11520118$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Imai, Hideki</creatorcontrib><creatorcontrib>Nishimura, Tsutomu</creatorcontrib><creatorcontrib>Sadamatsu, Miyuki</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Kabuto, Michinori</creatorcontrib><creatorcontrib>Kato, Nobumasa</creatorcontrib><title>Type II Glucocorticoid Receptors Are Involved in Neuronal Death and Astrocyte Activation Induced by Trimethyltin in the Rat Hippocampus</title><title>Experimental neurology</title><addtitle>Exp Neurol</addtitle><description>According to our previous study, trimethyltin (TMT), a neurotoxicant, induces the loss of pyramidal neurons in the rat hippocampus, which is preceded by a transient increase in plasma corticosterone concentration. To address whether this transient activation of the hypothalamopituitary–adrenocortical axis is related to neuronal loss in the hippocampus, we evaluated the effects of bilateral adrenalectomy (ADX) and the chronic supplemental treatment of glucocorticoid receptor agonists after ADX on TMT-induced hippocampal damage. Peroral administration of a single dose of TMT (9 mg/kg body wt) induced the extensive loss of CA3 pyramidal neurons and reactive astrocytosis in the hippocampus, as evidenced by results of vimentin and glial fibrillary acidic protein immunohistochemistry, and the effects were profoundly exacerbated by bilateral adrenalectomy. Prolonged administration of corticosterone not only attenuated the exacerbating effects of adrenalectomy but also partially reversed the TMT-induced neuronal loss and reactive astrocytosis. Dexamethasone, but not aldosterone, could be substituted for corticosterone, suggesting a novel neuroprotective action of type II glucocorticoid receptors in the hippocampus.</description><subject>Adrenalectomy</subject><subject>aldosterone</subject><subject>Aldosterone - pharmacology</subject><subject>Animals</subject><subject>Astrocytes - cytology</subject><subject>Astrocytes - drug effects</subject><subject>Astrocytes - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood. Blood coagulation. Reticuloendothelial system</subject><subject>Cell Count</subject><subject>Cell Death - drug effects</subject><subject>dexamethasone</subject><subject>Dexamethasone - pharmacology</subject><subject>Glial Fibrillary Acidic Protein - biosynthesis</subject><subject>Gliosis - chemically induced</subject><subject>Gliosis - pathology</subject><subject>Glucocorticoids - pharmacology</subject><subject>hippocampus</subject><subject>Hippocampus - cytology</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hypothalamo-Hypophyseal System - metabolism</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurons - cytology</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>Pharmacology. Drug treatments</subject><subject>Pituitary-Adrenal System - metabolism</subject><subject>Pyramidal Cells - cytology</subject><subject>Pyramidal Cells - drug effects</subject><subject>Pyramidal Cells - metabolism</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, Glucocorticoid - agonists</subject><subject>Receptors, Glucocorticoid - metabolism</subject><subject>trimethyltin</subject><subject>Trimethyltin Compounds - pharmacology</subject><subject>vimentin</subject><subject>Vimentin - biosynthesis</subject><issn>0014-4886</issn><issn>1090-2430</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2001</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFr2zAUgMXYWLNu1x2HLjs6e5JlWz6GbmsDpYOSnY3y9Ew0HMtIcph_Qf_2FBLoaSAQSN8nnj7GPgtYC4D6G_0dw1oCiHXTyOoNWwlooZCqhLdslY9VobSub9iHGP8AQKtk857dCFFJEEKv2MtumYhvt_x-mNGjD8mhd5Y_E9KUfIh8E_L9ePLDiSx3I3-iOfjRDPw7mXTgZrR8E1PwuCTiG0zuZJLzY3bsjFnZL3wX3JHSYRlS9vNKB-LPJvEHN00ezXGa40f2rjdDpE_X_Zb9_vljd_dQPP66395tHgtUZZ0K2_SW-j21CsteC6VtrZCor3UvAGXfmlqDAQRNUpS4l0rVdWXJtFUpVdWUt2x9eReDjzFQ3015OBOWTkB3Ltqdi3bnot25aBa-XIRp3h_JvuLXhBn4egVMRDP0wYzo4iunoNINtJnTF47y906OQhfR0ZgTuUCYOuvd_2b4BwMXlHI</recordid><startdate>20010901</startdate><enddate>20010901</enddate><creator>Imai, Hideki</creator><creator>Nishimura, Tsutomu</creator><creator>Sadamatsu, Miyuki</creator><creator>Liu, Ying</creator><creator>Kabuto, Michinori</creator><creator>Kato, Nobumasa</creator><general>Elsevier Inc</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></search><sort><creationdate>20010901</creationdate><title>Type II Glucocorticoid Receptors Are Involved in Neuronal Death and Astrocyte Activation Induced by Trimethyltin in the Rat Hippocampus</title><author>Imai, Hideki ; Nishimura, Tsutomu ; Sadamatsu, Miyuki ; Liu, Ying ; Kabuto, Michinori ; Kato, Nobumasa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-d7fdefbe94c3f8148d64ceef68f10c2f9a680a0c08e213cb244665dea95324573</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2001</creationdate><topic>Adrenalectomy</topic><topic>aldosterone</topic><topic>Aldosterone - pharmacology</topic><topic>Animals</topic><topic>Astrocytes - cytology</topic><topic>Astrocytes - drug effects</topic><topic>Astrocytes - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood. Blood coagulation. Reticuloendothelial system</topic><topic>Cell Count</topic><topic>Cell Death - drug effects</topic><topic>dexamethasone</topic><topic>Dexamethasone - pharmacology</topic><topic>Glial Fibrillary Acidic Protein - biosynthesis</topic><topic>Gliosis - chemically induced</topic><topic>Gliosis - pathology</topic><topic>Glucocorticoids - pharmacology</topic><topic>hippocampus</topic><topic>Hippocampus - cytology</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hypothalamo-Hypophyseal System - metabolism</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurons - cytology</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>Pharmacology. Drug treatments</topic><topic>Pituitary-Adrenal System - metabolism</topic><topic>Pyramidal Cells - cytology</topic><topic>Pyramidal Cells - drug effects</topic><topic>Pyramidal Cells - metabolism</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, Glucocorticoid - agonists</topic><topic>Receptors, Glucocorticoid - metabolism</topic><topic>trimethyltin</topic><topic>Trimethyltin Compounds - pharmacology</topic><topic>vimentin</topic><topic>Vimentin - biosynthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Imai, Hideki</creatorcontrib><creatorcontrib>Nishimura, Tsutomu</creatorcontrib><creatorcontrib>Sadamatsu, Miyuki</creatorcontrib><creatorcontrib>Liu, Ying</creatorcontrib><creatorcontrib>Kabuto, Michinori</creatorcontrib><creatorcontrib>Kato, Nobumasa</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><jtitle>Experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Imai, Hideki</au><au>Nishimura, Tsutomu</au><au>Sadamatsu, Miyuki</au><au>Liu, Ying</au><au>Kabuto, Michinori</au><au>Kato, Nobumasa</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Type II Glucocorticoid Receptors Are Involved in Neuronal Death and Astrocyte Activation Induced by Trimethyltin in the Rat Hippocampus</atitle><jtitle>Experimental neurology</jtitle><addtitle>Exp Neurol</addtitle><date>2001-09-01</date><risdate>2001</risdate><volume>171</volume><issue>1</issue><spage>22</spage><epage>28</epage><pages>22-28</pages><issn>0014-4886</issn><eissn>1090-2430</eissn><coden>EXNEAC</coden><abstract>According to our previous study, trimethyltin (TMT), a neurotoxicant, induces the loss of pyramidal neurons in the rat hippocampus, which is preceded by a transient increase in plasma corticosterone concentration. To address whether this transient activation of the hypothalamopituitary–adrenocortical axis is related to neuronal loss in the hippocampus, we evaluated the effects of bilateral adrenalectomy (ADX) and the chronic supplemental treatment of glucocorticoid receptor agonists after ADX on TMT-induced hippocampal damage. Peroral administration of a single dose of TMT (9 mg/kg body wt) induced the extensive loss of CA3 pyramidal neurons and reactive astrocytosis in the hippocampus, as evidenced by results of vimentin and glial fibrillary acidic protein immunohistochemistry, and the effects were profoundly exacerbated by bilateral adrenalectomy. Prolonged administration of corticosterone not only attenuated the exacerbating effects of adrenalectomy but also partially reversed the TMT-induced neuronal loss and reactive astrocytosis. Dexamethasone, but not aldosterone, could be substituted for corticosterone, suggesting a novel neuroprotective action of type II glucocorticoid receptors in the hippocampus.</abstract><cop>Amsterdam</cop><pub>Elsevier Inc</pub><pmid>11520118</pmid><doi>10.1006/exnr.2001.7725</doi><tpages>7</tpages></addata></record> |
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| ispartof | Experimental neurology, 2001-09, Vol.171 (1), p.22-28 |
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| subjects | Adrenalectomy aldosterone Aldosterone - pharmacology Animals Astrocytes - cytology Astrocytes - drug effects Astrocytes - metabolism Biological and medical sciences Blood. Blood coagulation. Reticuloendothelial system Cell Count Cell Death - drug effects dexamethasone Dexamethasone - pharmacology Glial Fibrillary Acidic Protein - biosynthesis Gliosis - chemically induced Gliosis - pathology Glucocorticoids - pharmacology hippocampus Hippocampus - cytology Hippocampus - drug effects Hippocampus - metabolism Hypothalamo-Hypophyseal System - metabolism Immunohistochemistry Male Medical sciences Neurons - cytology Neurons - drug effects Neurons - metabolism Pharmacology. Drug treatments Pituitary-Adrenal System - metabolism Pyramidal Cells - cytology Pyramidal Cells - drug effects Pyramidal Cells - metabolism Rats Rats, Sprague-Dawley Receptors, Glucocorticoid - agonists Receptors, Glucocorticoid - metabolism trimethyltin Trimethyltin Compounds - pharmacology vimentin Vimentin - biosynthesis |
| title | Type II Glucocorticoid Receptors Are Involved in Neuronal Death and Astrocyte Activation Induced by Trimethyltin in the Rat Hippocampus |
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