Kainate-induced seizures, oxidative stress and neuronal loss in aging rats
Abstract Aging is a significant risk factor for developing epilepsy. The mechanisms underlying age-related increase in seizure susceptibility and resultant injury remain unknown. Oxidative stress is an important mechanism that contributes to diverse age-related disorders. Whether age-related increas...
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| Veröffentlicht in: | Neuroscience 2007-07, Vol.147 (4), p.1114-1118 |
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| creator | Liang, L.P Beaudoin, M.E Fritz, M.J Fulton, R Patel, M |
| description | Abstract Aging is a significant risk factor for developing epilepsy. The mechanisms underlying age-related increase in seizure susceptibility and resultant injury remain unknown. Oxidative stress is an important mechanism that contributes to diverse age-related disorders. Whether age-related increased seizure susceptibility is accompanied by increased oxidative stress remains unknown. The goal of this study was to determine if aging per se increases the susceptibility of rats to kainate-induced behavioral seizures and oxidative stress. Adult (3–4 month-old) and aging (18–19 month-old) Sprague–Dawley rats were administered a single low dose of kainate (5 mg/kg, s.c.) or saline. Behavioral seizures were monitored in all four groups for a period for a period of ∼6 h. Oxidative stress (8-hydroxy-2′deoxyguanosine/2-deoxyguanosine; 8OHdG/2dG) was assessed 24 h following kainate injection. Stereological assessment of cell counts was performed in hippocampal tissue 7 days following kainate injection. In adult rats, administration of the low dose of kainate did not produce significant behavioral seizures, oxidative stress or cell loss. However, aging rats exhibited intense behavioral seizures consistent with status epilepticus following the low dose of kainate. In aging rats, kainate produced a significant increase in oxidative DNA damage (8OHdG/2dG) and neuronal loss in cornu ammonis regions 3 and 1 (CA3 and CA1), but not dentate gyrus compared with both age-matched controls and adult kainate-treated rats. These data suggest that the process of aging per se increases kainate-induced seizure susceptibility, oxidative stress and hippocampal pyramidal cell loss. |
| doi_str_mv | 10.1016/j.neuroscience.2007.03.026 |
| format | Article |
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The mechanisms underlying age-related increase in seizure susceptibility and resultant injury remain unknown. Oxidative stress is an important mechanism that contributes to diverse age-related disorders. Whether age-related increased seizure susceptibility is accompanied by increased oxidative stress remains unknown. The goal of this study was to determine if aging per se increases the susceptibility of rats to kainate-induced behavioral seizures and oxidative stress. Adult (3–4 month-old) and aging (18–19 month-old) Sprague–Dawley rats were administered a single low dose of kainate (5 mg/kg, s.c.) or saline. Behavioral seizures were monitored in all four groups for a period for a period of ∼6 h. Oxidative stress (8-hydroxy-2′deoxyguanosine/2-deoxyguanosine; 8OHdG/2dG) was assessed 24 h following kainate injection. Stereological assessment of cell counts was performed in hippocampal tissue 7 days following kainate injection. In adult rats, administration of the low dose of kainate did not produce significant behavioral seizures, oxidative stress or cell loss. However, aging rats exhibited intense behavioral seizures consistent with status epilepticus following the low dose of kainate. In aging rats, kainate produced a significant increase in oxidative DNA damage (8OHdG/2dG) and neuronal loss in cornu ammonis regions 3 and 1 (CA3 and CA1), but not dentate gyrus compared with both age-matched controls and adult kainate-treated rats. These data suggest that the process of aging per se increases kainate-induced seizure susceptibility, oxidative stress and hippocampal pyramidal cell loss.</description><identifier>ISSN: 0306-4522</identifier><identifier>EISSN: 1873-7544</identifier><identifier>DOI: 10.1016/j.neuroscience.2007.03.026</identifier><identifier>PMID: 17590518</identifier><identifier>CODEN: NRSCDN</identifier><language>eng</language><publisher>Oxford: Elsevier Ltd</publisher><subject>aging ; Aging - physiology ; Animals ; Behavior, Animal - drug effects ; Biological and medical sciences ; Cell Death - drug effects ; Deoxyguanosine - analogs & derivatives ; Deoxyguanosine - metabolism ; Dose-Response Relationship, Drug ; epilepsy ; Fundamental and applied biological sciences. Psychology ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; hippocampus ; Kainic Acid ; Male ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neurology ; neuronal death ; Neurons - drug effects ; Neurons - metabolism ; oxidative damage ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Rats, Sprague-Dawley ; Seizures - chemically induced ; Seizures - metabolism ; Seizures - pathology ; Severity of Illness Index ; Time Factors ; Vertebrates: nervous system and sense organs</subject><ispartof>Neuroscience, 2007-07, Vol.147 (4), p.1114-1118</ispartof><rights>IBRO</rights><rights>2007 IBRO</rights><rights>2007 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c494t-226160e6d39d180da705c0755d94867f3972f19c684559500e0861e50e62c60d3</citedby><cites>FETCH-LOGICAL-c494t-226160e6d39d180da705c0755d94867f3972f19c684559500e0861e50e62c60d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.neuroscience.2007.03.026$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,778,782,3539,27907,27908,45978</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18973678$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17590518$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liang, L.P</creatorcontrib><creatorcontrib>Beaudoin, M.E</creatorcontrib><creatorcontrib>Fritz, M.J</creatorcontrib><creatorcontrib>Fulton, R</creatorcontrib><creatorcontrib>Patel, M</creatorcontrib><title>Kainate-induced seizures, oxidative stress and neuronal loss in aging rats</title><title>Neuroscience</title><addtitle>Neuroscience</addtitle><description>Abstract Aging is a significant risk factor for developing epilepsy. The mechanisms underlying age-related increase in seizure susceptibility and resultant injury remain unknown. Oxidative stress is an important mechanism that contributes to diverse age-related disorders. Whether age-related increased seizure susceptibility is accompanied by increased oxidative stress remains unknown. The goal of this study was to determine if aging per se increases the susceptibility of rats to kainate-induced behavioral seizures and oxidative stress. Adult (3–4 month-old) and aging (18–19 month-old) Sprague–Dawley rats were administered a single low dose of kainate (5 mg/kg, s.c.) or saline. Behavioral seizures were monitored in all four groups for a period for a period of ∼6 h. Oxidative stress (8-hydroxy-2′deoxyguanosine/2-deoxyguanosine; 8OHdG/2dG) was assessed 24 h following kainate injection. Stereological assessment of cell counts was performed in hippocampal tissue 7 days following kainate injection. In adult rats, administration of the low dose of kainate did not produce significant behavioral seizures, oxidative stress or cell loss. However, aging rats exhibited intense behavioral seizures consistent with status epilepticus following the low dose of kainate. In aging rats, kainate produced a significant increase in oxidative DNA damage (8OHdG/2dG) and neuronal loss in cornu ammonis regions 3 and 1 (CA3 and CA1), but not dentate gyrus compared with both age-matched controls and adult kainate-treated rats. These data suggest that the process of aging per se increases kainate-induced seizure susceptibility, oxidative stress and hippocampal pyramidal cell loss.</description><subject>aging</subject><subject>Aging - physiology</subject><subject>Animals</subject><subject>Behavior, Animal - drug effects</subject><subject>Biological and medical sciences</subject><subject>Cell Death - drug effects</subject><subject>Deoxyguanosine - analogs & derivatives</subject><subject>Deoxyguanosine - metabolism</subject><subject>Dose-Response Relationship, Drug</subject><subject>epilepsy</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>hippocampus</subject><subject>Kainic Acid</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>neuronal death</subject><subject>Neurons - drug effects</subject><subject>Neurons - metabolism</subject><subject>oxidative damage</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Seizures - chemically induced</subject><subject>Seizures - metabolism</subject><subject>Seizures - pathology</subject><subject>Severity of Illness Index</subject><subject>Time Factors</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0306-4522</issn><issn>1873-7544</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkV2L1TAQhoMo7nH1L0gR9MrWyXfjhSDrtwteqNchJtMlx550TdrF9debegorXpmbwPDMvMkzhDyi0FGg6tm-S7jkqfiIyWPHAHQHvAOmbpEd7TVvtRTiNtkBB9UKydgJuVfKHuqRgt8lJ1RLA5L2O_Lho4vJzdjGFBaPoSkYfy0Zy9Nm-hmDm-MVNmWuhdK4FJo_ycmNzTjVSkyNu4jposluLvfJncGNBR9s9yn5-ub1l7N37fmnt-_PXp63Xhgxt4wpqgBV4CbQHoLTID1oKYMRvdIDN5oN1HjVCymNBEDoFUVZW5hXEPgpeXKce5mnHwuW2R5i8TiOLuG0FEuNNlRqVcHnR9BXWSXjYC9zPLh8bSnY1aTd279N2tWkBW6rydr8cEtZvh0w3LRu6irweANc8W4csks-lhuuN5orvXKvjhxWJ1cRs93iQszoZxum-H_vefHPGD_GFGvyd7zGsp-WXNdSf28Ls2A_r7tfVw8agAul-G-BuKwp</recordid><startdate>20070729</startdate><enddate>20070729</enddate><creator>Liang, L.P</creator><creator>Beaudoin, M.E</creator><creator>Fritz, M.J</creator><creator>Fulton, R</creator><creator>Patel, M</creator><general>Elsevier 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>7TM</scope></search><sort><creationdate>20070729</creationdate><title>Kainate-induced seizures, oxidative stress and neuronal loss in aging rats</title><author>Liang, L.P ; Beaudoin, M.E ; Fritz, M.J ; Fulton, R ; Patel, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c494t-226160e6d39d180da705c0755d94867f3972f19c684559500e0861e50e62c60d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>aging</topic><topic>Aging - physiology</topic><topic>Animals</topic><topic>Behavior, Animal - drug effects</topic><topic>Biological and medical sciences</topic><topic>Cell Death - drug effects</topic><topic>Deoxyguanosine - analogs & derivatives</topic><topic>Deoxyguanosine - metabolism</topic><topic>Dose-Response Relationship, Drug</topic><topic>epilepsy</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>hippocampus</topic><topic>Kainic Acid</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>neuronal death</topic><topic>Neurons - drug effects</topic><topic>Neurons - metabolism</topic><topic>oxidative damage</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Seizures - chemically induced</topic><topic>Seizures - metabolism</topic><topic>Seizures - pathology</topic><topic>Severity of Illness Index</topic><topic>Time Factors</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liang, L.P</creatorcontrib><creatorcontrib>Beaudoin, M.E</creatorcontrib><creatorcontrib>Fritz, M.J</creatorcontrib><creatorcontrib>Fulton, R</creatorcontrib><creatorcontrib>Patel, M</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>Nucleic Acids Abstracts</collection><jtitle>Neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liang, L.P</au><au>Beaudoin, M.E</au><au>Fritz, M.J</au><au>Fulton, R</au><au>Patel, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Kainate-induced seizures, oxidative stress and neuronal loss in aging rats</atitle><jtitle>Neuroscience</jtitle><addtitle>Neuroscience</addtitle><date>2007-07-29</date><risdate>2007</risdate><volume>147</volume><issue>4</issue><spage>1114</spage><epage>1118</epage><pages>1114-1118</pages><issn>0306-4522</issn><eissn>1873-7544</eissn><coden>NRSCDN</coden><abstract>Abstract Aging is a significant risk factor for developing epilepsy. The mechanisms underlying age-related increase in seizure susceptibility and resultant injury remain unknown. Oxidative stress is an important mechanism that contributes to diverse age-related disorders. Whether age-related increased seizure susceptibility is accompanied by increased oxidative stress remains unknown. The goal of this study was to determine if aging per se increases the susceptibility of rats to kainate-induced behavioral seizures and oxidative stress. Adult (3–4 month-old) and aging (18–19 month-old) Sprague–Dawley rats were administered a single low dose of kainate (5 mg/kg, s.c.) or saline. Behavioral seizures were monitored in all four groups for a period for a period of ∼6 h. Oxidative stress (8-hydroxy-2′deoxyguanosine/2-deoxyguanosine; 8OHdG/2dG) was assessed 24 h following kainate injection. Stereological assessment of cell counts was performed in hippocampal tissue 7 days following kainate injection. In adult rats, administration of the low dose of kainate did not produce significant behavioral seizures, oxidative stress or cell loss. However, aging rats exhibited intense behavioral seizures consistent with status epilepticus following the low dose of kainate. In aging rats, kainate produced a significant increase in oxidative DNA damage (8OHdG/2dG) and neuronal loss in cornu ammonis regions 3 and 1 (CA3 and CA1), but not dentate gyrus compared with both age-matched controls and adult kainate-treated rats. These data suggest that the process of aging per se increases kainate-induced seizure susceptibility, oxidative stress and hippocampal pyramidal cell loss.</abstract><cop>Oxford</cop><pub>Elsevier Ltd</pub><pmid>17590518</pmid><doi>10.1016/j.neuroscience.2007.03.026</doi><tpages>5</tpages></addata></record> |
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| subjects | aging Aging - physiology Animals Behavior, Animal - drug effects Biological and medical sciences Cell Death - drug effects Deoxyguanosine - analogs & derivatives Deoxyguanosine - metabolism Dose-Response Relationship, Drug epilepsy Fundamental and applied biological sciences. Psychology Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy hippocampus Kainic Acid Male Medical sciences Nervous system (semeiology, syndromes) Neurology neuronal death Neurons - drug effects Neurons - metabolism oxidative damage Oxidative Stress - drug effects Oxidative Stress - physiology Rats Rats, Sprague-Dawley Seizures - chemically induced Seizures - metabolism Seizures - pathology Severity of Illness Index Time Factors Vertebrates: nervous system and sense organs |
| title | Kainate-induced seizures, oxidative stress and neuronal loss in aging rats |
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