Quantitative Analysis of Delayed Neuronal Death in the Hippocampal Subfields of SHRSP and SHR
Transient forebrain ischemia and reperfusion induces delayed neuronal death (DND) in the hippocampal Cornu Ammonis 1 (CA1) subfield of stroke-prone spontaneously hypertensive rat (SHRSP). The vulnerability to DND is potentially related to the genetic susceptibility to stroke in this strain. To eluci...
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| Veröffentlicht in: | Cellular and molecular neurobiology 2009-06, Vol.29 (4), p.557-562 |
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| creator | Daisu, Mitsuhiro Hatta, Toshihisa Sakurai-Yamashita, Yasuko Nabika, Toru Moritake, Kouzo |
| description | Transient forebrain ischemia and reperfusion induces delayed neuronal death (DND) in the hippocampal Cornu Ammonis 1 (CA1) subfield of stroke-prone spontaneously hypertensive rat (SHRSP). The vulnerability to DND is potentially related to the genetic susceptibility to stroke in this strain. To elucidate the mechanism of DND in SHRSP, however, it is essential to establish a method for quantitative evaluation of DND, which is not available yet. Male SHRSPs and spontaneously hypertensive rats (SHRs) at 12 weeks of age were used in the experiment. The bilateral common carotid arteries were surgically occluded with aneurysmal clips for 10 min. The brain was taken out 7 days after the experiment of the transient ischemia, and was sliced into serial coronal sections. Quantitative estimation of the number of viable pyramidal cells in the CA1 and CA2/3 subfields was performed based on the stereology with a random and systematic sampling. The transient ischemia and reperfusion (TIR) significantly reduced the number of viable pyramidal cells in CA1 of SHRSP (61000 ± 20100 in TIR vs. 128500 ± 21900 in the sham-operation, P < 0.000001 by Student's t-test), while no significant difference was observed in SHR (140300 ± 30800 in TIR vs. 128200 ± 16700 in the sham-operation, P = 0.35). Further analysis revealed a dorsal-ventral gradient in the distribution of DND in CA1 of SHRSP with the most severe change in the dorsal area. The quantitative measurement using a stereological method is useful in the precise evaluation of DND in SHRSP. This method can be applied in the studies of effects of medical treatments on the 'ischemia/reperfusion' insult. |
| doi_str_mv | 10.1007/s10571-009-9347-9 |
| format | Article |
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The vulnerability to DND is potentially related to the genetic susceptibility to stroke in this strain. To elucidate the mechanism of DND in SHRSP, however, it is essential to establish a method for quantitative evaluation of DND, which is not available yet. Male SHRSPs and spontaneously hypertensive rats (SHRs) at 12 weeks of age were used in the experiment. The bilateral common carotid arteries were surgically occluded with aneurysmal clips for 10 min. The brain was taken out 7 days after the experiment of the transient ischemia, and was sliced into serial coronal sections. Quantitative estimation of the number of viable pyramidal cells in the CA1 and CA2/3 subfields was performed based on the stereology with a random and systematic sampling. The transient ischemia and reperfusion (TIR) significantly reduced the number of viable pyramidal cells in CA1 of SHRSP (61000 ± 20100 in TIR vs. 128500 ± 21900 in the sham-operation, P < 0.000001 by Student's t-test), while no significant difference was observed in SHR (140300 ± 30800 in TIR vs. 128200 ± 16700 in the sham-operation, P = 0.35). Further analysis revealed a dorsal-ventral gradient in the distribution of DND in CA1 of SHRSP with the most severe change in the dorsal area. The quantitative measurement using a stereological method is useful in the precise evaluation of DND in SHRSP. 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The vulnerability to DND is potentially related to the genetic susceptibility to stroke in this strain. To elucidate the mechanism of DND in SHRSP, however, it is essential to establish a method for quantitative evaluation of DND, which is not available yet. Male SHRSPs and spontaneously hypertensive rats (SHRs) at 12 weeks of age were used in the experiment. The bilateral common carotid arteries were surgically occluded with aneurysmal clips for 10 min. The brain was taken out 7 days after the experiment of the transient ischemia, and was sliced into serial coronal sections. Quantitative estimation of the number of viable pyramidal cells in the CA1 and CA2/3 subfields was performed based on the stereology with a random and systematic sampling. The transient ischemia and reperfusion (TIR) significantly reduced the number of viable pyramidal cells in CA1 of SHRSP (61000 ± 20100 in TIR vs. 128500 ± 21900 in the sham-operation, P < 0.000001 by Student's t-test), while no significant difference was observed in SHR (140300 ± 30800 in TIR vs. 128200 ± 16700 in the sham-operation, P = 0.35). Further analysis revealed a dorsal-ventral gradient in the distribution of DND in CA1 of SHRSP with the most severe change in the dorsal area. The quantitative measurement using a stereological method is useful in the precise evaluation of DND in SHRSP. This method can be applied in the studies of effects of medical treatments on the 'ischemia/reperfusion' insult.</description><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Biology</subject><subject>Cell Death - physiology</subject><subject>Hippocampus - anatomy & histology</subject><subject>Hippocampus - physiology</subject><subject>Male</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Pyramidal Cells - cytology</subject><subject>Pyramidal Cells - physiology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Stroke - pathology</subject><issn>0272-4340</issn><issn>1573-6830</issn><issn>1573-6830</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE1P3DAQhi3UCpYtP6CXNqdySjv-SGwfEYUuEurXliOyvPYEjLJJsJNK--_rbVbixsVjzfvMe3gIeU_hMwWQXxKFStISQJeaC1nqI7KgleRlrTi8IQtgkpWCCzghpyk9QQYBqmNyQjWVjGtYkPtfk-3GMNox_MXiorPtLoVU9E3xFVu7Q198xyn2eZ8XdnwsQleMj1iswjD0zm6HHKynTROw9f_P1qvf65-F7fz-9468bWyb8Owwl-Tu-urP5aq8_fHt5vLitnRcq7FELhmtqVKKOevrilVOOcG81JpJ0A6FaJTPCXUbXSMDEHQj0VPeMK8440tyPvcOsX-eMI1mG5LDtrUd9lMyshJKgxB1Jj-9StaSV0wznkE6gy72KUVszBDD1sadoWD29s1s32SpZm8_P0vy4VA-bbboXy4OujPAZiDlqHvAaJ76KWa56dXWj_NRY3tjH2JI5m7NgHKgtWC1EPwfs5iW-w</recordid><startdate>20090601</startdate><enddate>20090601</enddate><creator>Daisu, Mitsuhiro</creator><creator>Hatta, Toshihisa</creator><creator>Sakurai-Yamashita, Yasuko</creator><creator>Nabika, Toru</creator><creator>Moritake, Kouzo</creator><general>Boston : Springer US</general><general>Springer US</general><scope>FBQ</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>7X8</scope><scope>7TK</scope></search><sort><creationdate>20090601</creationdate><title>Quantitative Analysis of Delayed Neuronal Death in the Hippocampal Subfields of SHRSP and SHR</title><author>Daisu, Mitsuhiro ; Hatta, Toshihisa ; Sakurai-Yamashita, Yasuko ; Nabika, Toru ; Moritake, Kouzo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c398t-e3721618882cad6525c8c42d7992709ce44f8dad61cb96e20041b7ed13f2d8323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Biology</topic><topic>Cell Death - physiology</topic><topic>Hippocampus - anatomy & histology</topic><topic>Hippocampus - physiology</topic><topic>Male</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Pyramidal Cells - cytology</topic><topic>Pyramidal Cells - physiology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Stroke - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Daisu, Mitsuhiro</creatorcontrib><creatorcontrib>Hatta, Toshihisa</creatorcontrib><creatorcontrib>Sakurai-Yamashita, Yasuko</creatorcontrib><creatorcontrib>Nabika, Toru</creatorcontrib><creatorcontrib>Moritake, Kouzo</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Neurosciences Abstracts</collection><jtitle>Cellular and molecular neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Daisu, Mitsuhiro</au><au>Hatta, Toshihisa</au><au>Sakurai-Yamashita, Yasuko</au><au>Nabika, Toru</au><au>Moritake, Kouzo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Quantitative Analysis of Delayed Neuronal Death in the Hippocampal Subfields of SHRSP and SHR</atitle><jtitle>Cellular and molecular neurobiology</jtitle><stitle>Cell Mol Neurobiol</stitle><addtitle>Cell Mol Neurobiol</addtitle><date>2009-06-01</date><risdate>2009</risdate><volume>29</volume><issue>4</issue><spage>557</spage><epage>562</epage><pages>557-562</pages><issn>0272-4340</issn><issn>1573-6830</issn><eissn>1573-6830</eissn><abstract>Transient forebrain ischemia and reperfusion induces delayed neuronal death (DND) in the hippocampal Cornu Ammonis 1 (CA1) subfield of stroke-prone spontaneously hypertensive rat (SHRSP). The vulnerability to DND is potentially related to the genetic susceptibility to stroke in this strain. To elucidate the mechanism of DND in SHRSP, however, it is essential to establish a method for quantitative evaluation of DND, which is not available yet. Male SHRSPs and spontaneously hypertensive rats (SHRs) at 12 weeks of age were used in the experiment. The bilateral common carotid arteries were surgically occluded with aneurysmal clips for 10 min. The brain was taken out 7 days after the experiment of the transient ischemia, and was sliced into serial coronal sections. Quantitative estimation of the number of viable pyramidal cells in the CA1 and CA2/3 subfields was performed based on the stereology with a random and systematic sampling. The transient ischemia and reperfusion (TIR) significantly reduced the number of viable pyramidal cells in CA1 of SHRSP (61000 ± 20100 in TIR vs. 128500 ± 21900 in the sham-operation, P < 0.000001 by Student's t-test), while no significant difference was observed in SHR (140300 ± 30800 in TIR vs. 128200 ± 16700 in the sham-operation, P = 0.35). Further analysis revealed a dorsal-ventral gradient in the distribution of DND in CA1 of SHRSP with the most severe change in the dorsal area. The quantitative measurement using a stereological method is useful in the precise evaluation of DND in SHRSP. This method can be applied in the studies of effects of medical treatments on the 'ischemia/reperfusion' insult.</abstract><cop>Boston</cop><pub>Boston : Springer US</pub><pmid>19172390</pmid><doi>10.1007/s10571-009-9347-9</doi><tpages>6</tpages></addata></record> |
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| subjects | Animals Biomedical and Life Sciences Biomedicine Cell Biology Cell Death - physiology Hippocampus - anatomy & histology Hippocampus - physiology Male Neurobiology Neurosciences Original Paper Pyramidal Cells - cytology Pyramidal Cells - physiology Rats Rats, Inbred SHR Stroke - pathology |
| title | Quantitative Analysis of Delayed Neuronal Death in the Hippocampal Subfields of SHRSP and SHR |
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