Distinct Types of Microglial Activation in White and Grey Matter of Rat Lumbosacral Cord After Mid-Thoracic Spinal Transection
The inflammatory response has been characterized in the lumbosacral segments (L4-S1) of rats after spinal transection at T8. Immune cells were identified immunohistochemically using antibodies to complement type 3 receptor, CD11b (OX-42), the macrophage lysosomal antigen, CD68 (ED1), major histocomp...
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Veröffentlicht in: | Journal of neuropathology and experimental neurology 2007-08, Vol.66 (8), p.698-710 |
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description | The inflammatory response has been characterized in the lumbosacral segments (L4-S1) of rats after spinal transection at T8. Immune cells were identified immunohistochemically using antibodies to complement type 3 receptor, CD11b (OX-42), the macrophage lysosomal antigen, CD68 (ED1), major histocompatibility complex class II (MHC II), and CD163 (ED2), a marker of perivascular cells. One week after cord transection, OX-42+ microglial density had nearly doubled. In the white matter, microglia became enlarged, often with retracted processes. In contrast, microglia in the grey matter remained ramified although nearly half of those lying medially contained clusters of ED1+ granules. After 8 weeks, ED1+ (+/−MHC II) macrophages were prominent in regions of Wallerian degeneration extending from dorsolateral to ventral funiculi. Microglial density remained raised in grey matter, particularly in the ventral horns of L4/5. Ramified microglia expressing MHC II+ (+/−ED1) extended from deep in the dorsal columns and around the central canal to the ventral columns. More ED2+ (+/−MHC II) perivascular and meningeal cells were recruited and expressed ED1. Thus, distinct from their conversion into macrophages in the white matter, the activation of ramified microglia after degeneration in the grey matter involves expression of ED1 without morphologic transformation. |
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Immune cells were identified immunohistochemically using antibodies to complement type 3 receptor, CD11b (OX-42), the macrophage lysosomal antigen, CD68 (ED1), major histocompatibility complex class II (MHC II), and CD163 (ED2), a marker of perivascular cells. One week after cord transection, OX-42+ microglial density had nearly doubled. In the white matter, microglia became enlarged, often with retracted processes. In contrast, microglia in the grey matter remained ramified although nearly half of those lying medially contained clusters of ED1+ granules. After 8 weeks, ED1+ (+/−MHC II) macrophages were prominent in regions of Wallerian degeneration extending from dorsolateral to ventral funiculi. Microglial density remained raised in grey matter, particularly in the ventral horns of L4/5. Ramified microglia expressing MHC II+ (+/−ED1) extended from deep in the dorsal columns and around the central canal to the ventral columns. More ED2+ (+/−MHC II) perivascular and meningeal cells were recruited and expressed ED1. Thus, distinct from their conversion into macrophages in the white matter, the activation of ramified microglia after degeneration in the grey matter involves expression of ED1 without morphologic transformation.</description><identifier>ISSN: 0022-3069</identifier><identifier>EISSN: 1554-6578</identifier><identifier>DOI: 10.1097/nen.0b013e3181256b32</identifier><identifier>PMID: 17882014</identifier><identifier>CODEN: JNENAD</identifier><language>eng</language><publisher>Hagerstown, MD: American Association of Neuropathologists, Inc</publisher><subject>Animals ; Biological and medical sciences ; CD11b Antigen - metabolism ; Cell Count ; Diseases of striated muscles. Neuromuscular diseases ; Ectodysplasins - metabolism ; Female ; Histocompatibility Antigens Class II - metabolism ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Lumbosacral Region - pathology ; Medical sciences ; Microglia - classification ; Microglia - metabolism ; Microglia - pathology ; Myelin Basic Protein - metabolism ; Nerve Tissue - pathology ; Neurology ; Rats ; Rats, Wistar ; Spinal Cord Injuries - metabolism ; Spinal Cord Injuries - pathology ; Thoracic Vertebrae ; Time Factors ; Traumas. Diseases due to physical agents</subject><ispartof>Journal of neuropathology and experimental neurology, 2007-08, Vol.66 (8), p.698-710</ispartof><rights>2007 American Association of Neuropathologists, Inc</rights><rights>2007 INIST-CNRS</rights><rights>Copyright Lippincott Williams & Wilkins Aug 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4844-94e56442a308607962dbefe967c55f91ed2629cea8af6ee5c783de4fc990aa723</citedby><cites>FETCH-LOGICAL-c4844-94e56442a308607962dbefe967c55f91ed2629cea8af6ee5c783de4fc990aa723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18986815$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17882014$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>McKay, Sarah M</creatorcontrib><creatorcontrib>Brooks, Daniel J</creatorcontrib><creatorcontrib>Hu, Ping</creatorcontrib><creatorcontrib>McLachlan, Elspeth M</creatorcontrib><title>Distinct Types of Microglial Activation in White and Grey Matter of Rat Lumbosacral Cord After Mid-Thoracic Spinal Transection</title><title>Journal of neuropathology and experimental neurology</title><addtitle>J Neuropathol Exp Neurol</addtitle><description>The inflammatory response has been characterized in the lumbosacral segments (L4-S1) of rats after spinal transection at T8. Immune cells were identified immunohistochemically using antibodies to complement type 3 receptor, CD11b (OX-42), the macrophage lysosomal antigen, CD68 (ED1), major histocompatibility complex class II (MHC II), and CD163 (ED2), a marker of perivascular cells. One week after cord transection, OX-42+ microglial density had nearly doubled. In the white matter, microglia became enlarged, often with retracted processes. In contrast, microglia in the grey matter remained ramified although nearly half of those lying medially contained clusters of ED1+ granules. After 8 weeks, ED1+ (+/−MHC II) macrophages were prominent in regions of Wallerian degeneration extending from dorsolateral to ventral funiculi. Microglial density remained raised in grey matter, particularly in the ventral horns of L4/5. Ramified microglia expressing MHC II+ (+/−ED1) extended from deep in the dorsal columns and around the central canal to the ventral columns. More ED2+ (+/−MHC II) perivascular and meningeal cells were recruited and expressed ED1. Thus, distinct from their conversion into macrophages in the white matter, the activation of ramified microglia after degeneration in the grey matter involves expression of ED1 without morphologic transformation.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>CD11b Antigen - metabolism</subject><subject>Cell Count</subject><subject>Diseases of striated muscles. Neuromuscular diseases</subject><subject>Ectodysplasins - metabolism</subject><subject>Female</subject><subject>Histocompatibility Antigens Class II - metabolism</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Lumbosacral Region - pathology</subject><subject>Medical sciences</subject><subject>Microglia - classification</subject><subject>Microglia - metabolism</subject><subject>Microglia - pathology</subject><subject>Myelin Basic Protein - metabolism</subject><subject>Nerve Tissue - pathology</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Spinal Cord Injuries - metabolism</subject><subject>Spinal Cord Injuries - pathology</subject><subject>Thoracic Vertebrae</subject><subject>Time Factors</subject><subject>Traumas. Diseases due to physical agents</subject><issn>0022-3069</issn><issn>1554-6578</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFkl2L1DAYhYso7uzqPxAJgnvX9c1H83E5jLoKMwg64mVJ07dO1k47JqnL3PjbTdmBgb3xKiTvc07IOSmKVxRuKBj1bsDhBhqgHDnVlFWy4exJsaBVJUpZKf20WAAwVnKQ5qK4jPEOAAwY8by4oEprBlQsir_vfUx-cIlsjweMZOzIxrsw_uy97cnSJf_HJj8OxA_kx84nJHZoyW3AI9nYlDDMiq82kfW0b8ZoXciy1Rhasuzm6ca35XY3Buu8I98OfsjjbbBDRDfbviiedbaP-PK0XhXfP37Yrj6V6y-3n1fLdemEFqI0AispBLMctARlJGsb7NBI5aqqMxRbJplxaLXtJGLllOYtis4ZA9Yqxq-K6wffQxh_TxhTvffRYd_bAccp1lIzQ6Xh_wWpETlQTjP45hF4N04hPy_WjBnFJRUqQ-IByonGGLCrD8HvbTjWFOq5xTq3WD9uMcten7ynZo_tWXSqLQNvT4CNzvZdDtT5eOa00VLT6nz__djnNuKvfrrHUO_Q9mlX5_8AFShWMgAFOu_K-Ujwf1VAtcw</recordid><startdate>200708</startdate><enddate>200708</enddate><creator>McKay, Sarah M</creator><creator>Brooks, Daniel J</creator><creator>Hu, Ping</creator><creator>McLachlan, Elspeth M</creator><general>American Association of Neuropathologists, Inc</general><general>Lippincott Williams & Wilkins</general><general>Oxford University Press</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>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>88I</scope><scope>8AF</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>S0X</scope><scope>7TK</scope><scope>7X8</scope></search><sort><creationdate>200708</creationdate><title>Distinct Types of Microglial Activation in White and Grey Matter of Rat Lumbosacral Cord After Mid-Thoracic Spinal Transection</title><author>McKay, Sarah M ; Brooks, Daniel J ; Hu, Ping ; McLachlan, Elspeth M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4844-94e56442a308607962dbefe967c55f91ed2629cea8af6ee5c783de4fc990aa723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>CD11b Antigen - metabolism</topic><topic>Cell Count</topic><topic>Diseases of striated muscles. Neuromuscular diseases</topic><topic>Ectodysplasins - metabolism</topic><topic>Female</topic><topic>Histocompatibility Antigens Class II - metabolism</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Lumbosacral Region - pathology</topic><topic>Medical sciences</topic><topic>Microglia - classification</topic><topic>Microglia - metabolism</topic><topic>Microglia - pathology</topic><topic>Myelin Basic Protein - metabolism</topic><topic>Nerve Tissue - pathology</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Spinal Cord Injuries - metabolism</topic><topic>Spinal Cord Injuries - pathology</topic><topic>Thoracic Vertebrae</topic><topic>Time Factors</topic><topic>Traumas. Diseases due to physical agents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>McKay, Sarah M</creatorcontrib><creatorcontrib>Brooks, Daniel J</creatorcontrib><creatorcontrib>Hu, Ping</creatorcontrib><creatorcontrib>McLachlan, Elspeth 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>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>SIRS Editorial</collection><collection>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of neuropathology and experimental neurology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>McKay, Sarah M</au><au>Brooks, Daniel J</au><au>Hu, Ping</au><au>McLachlan, Elspeth M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Distinct Types of Microglial Activation in White and Grey Matter of Rat Lumbosacral Cord After Mid-Thoracic Spinal Transection</atitle><jtitle>Journal of neuropathology and experimental neurology</jtitle><addtitle>J Neuropathol Exp Neurol</addtitle><date>2007-08</date><risdate>2007</risdate><volume>66</volume><issue>8</issue><spage>698</spage><epage>710</epage><pages>698-710</pages><issn>0022-3069</issn><eissn>1554-6578</eissn><coden>JNENAD</coden><abstract>The inflammatory response has been characterized in the lumbosacral segments (L4-S1) of rats after spinal transection at T8. Immune cells were identified immunohistochemically using antibodies to complement type 3 receptor, CD11b (OX-42), the macrophage lysosomal antigen, CD68 (ED1), major histocompatibility complex class II (MHC II), and CD163 (ED2), a marker of perivascular cells. One week after cord transection, OX-42+ microglial density had nearly doubled. In the white matter, microglia became enlarged, often with retracted processes. In contrast, microglia in the grey matter remained ramified although nearly half of those lying medially contained clusters of ED1+ granules. After 8 weeks, ED1+ (+/−MHC II) macrophages were prominent in regions of Wallerian degeneration extending from dorsolateral to ventral funiculi. Microglial density remained raised in grey matter, particularly in the ventral horns of L4/5. Ramified microglia expressing MHC II+ (+/−ED1) extended from deep in the dorsal columns and around the central canal to the ventral columns. More ED2+ (+/−MHC II) perivascular and meningeal cells were recruited and expressed ED1. Thus, distinct from their conversion into macrophages in the white matter, the activation of ramified microglia after degeneration in the grey matter involves expression of ED1 without morphologic transformation.</abstract><cop>Hagerstown, MD</cop><pub>American Association of Neuropathologists, Inc</pub><pmid>17882014</pmid><doi>10.1097/nen.0b013e3181256b32</doi><tpages>13</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences CD11b Antigen - metabolism Cell Count Diseases of striated muscles. Neuromuscular diseases Ectodysplasins - metabolism Female Histocompatibility Antigens Class II - metabolism Injuries of the nervous system and the skull. Diseases due to physical agents Lumbosacral Region - pathology Medical sciences Microglia - classification Microglia - metabolism Microglia - pathology Myelin Basic Protein - metabolism Nerve Tissue - pathology Neurology Rats Rats, Wistar Spinal Cord Injuries - metabolism Spinal Cord Injuries - pathology Thoracic Vertebrae Time Factors Traumas. Diseases due to physical agents |
title | Distinct Types of Microglial Activation in White and Grey Matter of Rat Lumbosacral Cord After Mid-Thoracic Spinal Transection |
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