Oligodendrocyte Vulnerability Following Traumatic Brain Injury in Rats: Effect of Moderate Hypothermia
The purpose of this study was to document patterns of oligodendrocyte vulnerability to traumatic brain injury (TBI) and determine whether post-traumatic hypothermia prevents oligodendrocyte cell loss. Sprague-Dawley rats underwent moderate fluid percussion brain injury. Thirty minutes after TBI, bra...
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| Veröffentlicht in: | Therapeutic hypothermia and temperature management 2011-03, Vol.1 (1), p.43-51 |
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| creator | Lotocki, George Vaccari, Juan de Rivero Alonso, Ofelia Molano, Juliana Sanchez Nixon, Ryan Dietrich, W. Dalton Bramlett, Helen M. |
| description | The purpose of this study was to document patterns of oligodendrocyte vulnerability to traumatic brain injury (TBI) and determine whether post-traumatic hypothermia prevents oligodendrocyte cell loss. Sprague-Dawley rats underwent moderate fluid percussion brain injury. Thirty minutes after TBI, brain temperature was reduced to 33°C for 4 hours or maintained at normothermic levels (37°C). Animals were perfusion-fixed for quantitative immunohistochemical analysis at 3 (
n
= 9) or 7 (
n
= 9) days post-TBI. Within the cerebral cortex, external capsule, and corpus callosum, numbers of APC-CC1 immunoreactive oligodendrocytes at 3 and 7 days following TBI were significantly decreased compared with sham-operated rats (
p
|
| doi_str_mv | 10.1089/ther.2010.0011 |
| format | Article |
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n
= 9) or 7 (
n
= 9) days post-TBI. Within the cerebral cortex, external capsule, and corpus callosum, numbers of APC-CC1 immunoreactive oligodendrocytes at 3 and 7 days following TBI were significantly decreased compared with sham-operated rats (
p
< 0.02). Double-labeling studies showed that vulnerable oligodendrocytes expressed increased Caspase 3 activation compared with sham. Post-traumatic hypothermia significantly reduced the number of CC1-positive oligodendrocytes lost after normothermia TBI in white matter tracts (
p
< 0.01). This model of TBI leads to quantifiable regional patterns of oligodendrocyte vulnerability. Post-traumatic hypothermia protects oligodendrocytes by interfering with Caspase 3-mediated cell death mechanisms. Therapeutic hypothermia may improve functional outcome by attenuating trauma-induced oligodendrocyte cell death, subsequent demyelination, and circuit dysfunction.</description><identifier>ISSN: 2153-7658</identifier><identifier>EISSN: 2153-7933</identifier><identifier>DOI: 10.1089/ther.2010.0011</identifier><identifier>PMID: 23336085</identifier><language>eng</language><publisher>United States: Mary Ann Liebert, Inc</publisher><subject>Apoptosis ; Original ; Original Articles ; Rodents ; Traumatic brain injury</subject><ispartof>Therapeutic hypothermia and temperature management, 2011-03, Vol.1 (1), p.43-51</ispartof><rights>2011, Mary Ann Liebert, Inc.</rights><rights>(©) Copyright 2011, Mary Ann Liebert, Inc.</rights><rights>Copyright 2011, Mary Ann Liebert, Inc. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c393t-5862d31f326abbbb4d1e798428d371a67648de0b726f136f254a747b164d7d6c3</citedby><cites>FETCH-LOGICAL-c393t-5862d31f326abbbb4d1e798428d371a67648de0b726f136f254a747b164d7d6c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23336085$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lotocki, George</creatorcontrib><creatorcontrib>Vaccari, Juan de Rivero</creatorcontrib><creatorcontrib>Alonso, Ofelia</creatorcontrib><creatorcontrib>Molano, Juliana Sanchez</creatorcontrib><creatorcontrib>Nixon, Ryan</creatorcontrib><creatorcontrib>Dietrich, W. Dalton</creatorcontrib><creatorcontrib>Bramlett, Helen M.</creatorcontrib><title>Oligodendrocyte Vulnerability Following Traumatic Brain Injury in Rats: Effect of Moderate Hypothermia</title><title>Therapeutic hypothermia and temperature management</title><addtitle>Ther Hypothermia Temp Manag</addtitle><description>The purpose of this study was to document patterns of oligodendrocyte vulnerability to traumatic brain injury (TBI) and determine whether post-traumatic hypothermia prevents oligodendrocyte cell loss. Sprague-Dawley rats underwent moderate fluid percussion brain injury. Thirty minutes after TBI, brain temperature was reduced to 33°C for 4 hours or maintained at normothermic levels (37°C). Animals were perfusion-fixed for quantitative immunohistochemical analysis at 3 (
n
= 9) or 7 (
n
= 9) days post-TBI. Within the cerebral cortex, external capsule, and corpus callosum, numbers of APC-CC1 immunoreactive oligodendrocytes at 3 and 7 days following TBI were significantly decreased compared with sham-operated rats (
p
< 0.02). Double-labeling studies showed that vulnerable oligodendrocytes expressed increased Caspase 3 activation compared with sham. Post-traumatic hypothermia significantly reduced the number of CC1-positive oligodendrocytes lost after normothermia TBI in white matter tracts (
p
< 0.01). This model of TBI leads to quantifiable regional patterns of oligodendrocyte vulnerability. Post-traumatic hypothermia protects oligodendrocytes by interfering with Caspase 3-mediated cell death mechanisms. Therapeutic hypothermia may improve functional outcome by attenuating trauma-induced oligodendrocyte cell death, subsequent demyelination, and circuit dysfunction.</description><subject>Apoptosis</subject><subject>Original</subject><subject>Original Articles</subject><subject>Rodents</subject><subject>Traumatic brain injury</subject><issn>2153-7658</issn><issn>2153-7933</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNqFkc9rHSEQx5fS0oQ01x6D0Esv79Vfq24OhSYkTSAlUNJexV31xYerr-om7H9fl5eEtpfOZcbx45cZv03zHsE1gqL7VO5NWmNYjxAi9Ko5xKglK94R8vq5Zq04aI5z3sIaFGLKyNvmABNCGBTtYWNvvdtEbYJOcZiLAT8nH0xSvfOuzOAyeh8fXdiAu6SmURU3gLOkXADXYTulGdTquyr5FFxYa4YCogXfqlxSVepq3sVlxNGpd80bq3w2x0_5qPlxeXF3frW6uf16ff7lZjWQjpRVKxjWBFmCmeprUI0M7wTFQhOOFOOMCm1gzzGziDCLW6o45T1iVHPNBnLUfN7r7qZ-NHowoSTl5S65UaVZRuXk3zfB3ctNfJCkpZx0ogp8fBJI8ddkcpGjy4PxXgUTpyyRwKzlEAle0Q__oNs4pVDXqxSELaIYkkqt99SQYs7J2JdhEJSLi3L5Irm4KBcX64OTP1d4wZ89qwDdA0tbheCd6U0q_9P9DQklqv8</recordid><startdate>20110301</startdate><enddate>20110301</enddate><creator>Lotocki, George</creator><creator>Vaccari, Juan de Rivero</creator><creator>Alonso, Ofelia</creator><creator>Molano, Juliana Sanchez</creator><creator>Nixon, Ryan</creator><creator>Dietrich, W. Dalton</creator><creator>Bramlett, Helen M.</creator><general>Mary Ann Liebert, Inc</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20110301</creationdate><title>Oligodendrocyte Vulnerability Following Traumatic Brain Injury in Rats: Effect of Moderate Hypothermia</title><author>Lotocki, George ; Vaccari, Juan de Rivero ; Alonso, Ofelia ; Molano, Juliana Sanchez ; Nixon, Ryan ; Dietrich, W. Dalton ; Bramlett, Helen M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c393t-5862d31f326abbbb4d1e798428d371a67648de0b726f136f254a747b164d7d6c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Apoptosis</topic><topic>Original</topic><topic>Original Articles</topic><topic>Rodents</topic><topic>Traumatic brain injury</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lotocki, George</creatorcontrib><creatorcontrib>Vaccari, Juan de Rivero</creatorcontrib><creatorcontrib>Alonso, Ofelia</creatorcontrib><creatorcontrib>Molano, Juliana Sanchez</creatorcontrib><creatorcontrib>Nixon, Ryan</creatorcontrib><creatorcontrib>Dietrich, W. Dalton</creatorcontrib><creatorcontrib>Bramlett, Helen M.</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Therapeutic hypothermia and temperature management</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lotocki, George</au><au>Vaccari, Juan de Rivero</au><au>Alonso, Ofelia</au><au>Molano, Juliana Sanchez</au><au>Nixon, Ryan</au><au>Dietrich, W. Dalton</au><au>Bramlett, Helen M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oligodendrocyte Vulnerability Following Traumatic Brain Injury in Rats: Effect of Moderate Hypothermia</atitle><jtitle>Therapeutic hypothermia and temperature management</jtitle><addtitle>Ther Hypothermia Temp Manag</addtitle><date>2011-03-01</date><risdate>2011</risdate><volume>1</volume><issue>1</issue><spage>43</spage><epage>51</epage><pages>43-51</pages><issn>2153-7658</issn><eissn>2153-7933</eissn><abstract>The purpose of this study was to document patterns of oligodendrocyte vulnerability to traumatic brain injury (TBI) and determine whether post-traumatic hypothermia prevents oligodendrocyte cell loss. Sprague-Dawley rats underwent moderate fluid percussion brain injury. Thirty minutes after TBI, brain temperature was reduced to 33°C for 4 hours or maintained at normothermic levels (37°C). Animals were perfusion-fixed for quantitative immunohistochemical analysis at 3 (
n
= 9) or 7 (
n
= 9) days post-TBI. Within the cerebral cortex, external capsule, and corpus callosum, numbers of APC-CC1 immunoreactive oligodendrocytes at 3 and 7 days following TBI were significantly decreased compared with sham-operated rats (
p
< 0.02). Double-labeling studies showed that vulnerable oligodendrocytes expressed increased Caspase 3 activation compared with sham. Post-traumatic hypothermia significantly reduced the number of CC1-positive oligodendrocytes lost after normothermia TBI in white matter tracts (
p
< 0.01). This model of TBI leads to quantifiable regional patterns of oligodendrocyte vulnerability. Post-traumatic hypothermia protects oligodendrocytes by interfering with Caspase 3-mediated cell death mechanisms. Therapeutic hypothermia may improve functional outcome by attenuating trauma-induced oligodendrocyte cell death, subsequent demyelination, and circuit dysfunction.</abstract><cop>United States</cop><pub>Mary Ann Liebert, Inc</pub><pmid>23336085</pmid><doi>10.1089/ther.2010.0011</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| source | Alma/SFX Local Collection |
| subjects | Apoptosis Original Original Articles Rodents Traumatic brain injury |
| title | Oligodendrocyte Vulnerability Following Traumatic Brain Injury in Rats: Effect of Moderate Hypothermia |
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