p75NTR independent oligodendrocyte death in cuprizone-induced demyelination in C57BL/6 mice
Feeding C57Bl/6 J mice the copper chelator cuprizone leads to selective apoptosis of mature oligodendrocytes and concomitant demyelination predominantly in the corpus callosum. The process of oligodendrocyte apoptosis in this animal model for multiple sclerosis (MS) involves early microglial activat...
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creator | Copray, J. C. V. M. Küst, B. M. Mantingh-Otter, I. Boddeke, H. W. G. M. |
description | Feeding C57Bl/6 J mice the copper chelator cuprizone leads to selective apoptosis of mature oligodendrocytes and concomitant demyelination predominantly in the corpus callosum. The process of oligodendrocyte apoptosis in this animal model for multiple sclerosis (MS) involves early microglial activation, but no infiltration of T‐lymphocytes. Therefore, this model could mimic early stages of oligodendrocyte degeneration Affected oligodendrocytes express the common neurotrophin receptor, p75NTR, a ‘stress‐receptor’ which under certain circumstances can induce apoptosis. Only affected oligodendrocytes in MS lesions and MS animal models express this receptor. In order to study the significance of p75NTR in the fate of oligodendrocytes, we have exposed wild‐type as well as p75NTR‐knockout mice to a 0.2% (w/w) cuprizone diet and performed a comparative immunohistochemical analysis of the corpus callosum at various time points. Surprisingly, our results show that the absence of p75NTR did not alter cuprizone‐induced oligodendrocyte death (and subsequent de‐ or remyelination). Apparently, intracellular apoptosis pathways in adult oligodendrocytes do not require p75NTR activated signal transduction in the absence of T‐lymphocytes and T‐lymphocyte derived cytokines. |
doi_str_mv | 10.1111/j.1365-2990.2005.00656.x |
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C. V. M. ; Küst, B. M. ; Mantingh-Otter, I. ; Boddeke, H. W. G. M.</creator><creatorcontrib>Copray, J. C. V. M. ; Küst, B. M. ; Mantingh-Otter, I. ; Boddeke, H. W. G. M.</creatorcontrib><description>Feeding C57Bl/6 J mice the copper chelator cuprizone leads to selective apoptosis of mature oligodendrocytes and concomitant demyelination predominantly in the corpus callosum. The process of oligodendrocyte apoptosis in this animal model for multiple sclerosis (MS) involves early microglial activation, but no infiltration of T‐lymphocytes. Therefore, this model could mimic early stages of oligodendrocyte degeneration Affected oligodendrocytes express the common neurotrophin receptor, p75NTR, a ‘stress‐receptor’ which under certain circumstances can induce apoptosis. Only affected oligodendrocytes in MS lesions and MS animal models express this receptor. In order to study the significance of p75NTR in the fate of oligodendrocytes, we have exposed wild‐type as well as p75NTR‐knockout mice to a 0.2% (w/w) cuprizone diet and performed a comparative immunohistochemical analysis of the corpus callosum at various time points. Surprisingly, our results show that the absence of p75NTR did not alter cuprizone‐induced oligodendrocyte death (and subsequent de‐ or remyelination). Apparently, intracellular apoptosis pathways in adult oligodendrocytes do not require p75NTR activated signal transduction in the absence of T‐lymphocytes and T‐lymphocyte derived cytokines.</description><identifier>ISSN: 0305-1846</identifier><identifier>EISSN: 1365-2990</identifier><identifier>DOI: 10.1111/j.1365-2990.2005.00656.x</identifier><identifier>PMID: 16281908</identifier><identifier>CODEN: NANEDL</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Science Ltd</publisher><subject>Animals ; Apoptosis ; Biological and medical sciences ; central nervous system ; corpus callosum ; Corpus Callosum - pathology ; Cuprizone ; Demyelinating Diseases - chemically induced ; Demyelinating Diseases - pathology ; Demyelinating Diseases - physiopathology ; Human viral diseases ; immunohistochemistry ; Infectious diseases ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; Medical sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Monoamine Oxidase Inhibitors ; multiple sclerosis ; Nerve Regeneration ; Neurology ; neurotrophin receptor ; oligodendrocyte ; Oligodendroglia - pathology ; Receptor, Nerve Growth Factor - genetics ; T-Lymphocytes - pathology ; Traumas. Diseases due to physical agents ; Viral diseases ; Viral diseases of the lymphoid tissue and the blood. 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C. V. M.</creatorcontrib><creatorcontrib>Küst, B. M.</creatorcontrib><creatorcontrib>Mantingh-Otter, I.</creatorcontrib><creatorcontrib>Boddeke, H. W. G. M.</creatorcontrib><title>p75NTR independent oligodendrocyte death in cuprizone-induced demyelination in C57BL/6 mice</title><title>Neuropathology and applied neurobiology</title><addtitle>Neuropathol Appl Neurobiol</addtitle><description>Feeding C57Bl/6 J mice the copper chelator cuprizone leads to selective apoptosis of mature oligodendrocytes and concomitant demyelination predominantly in the corpus callosum. The process of oligodendrocyte apoptosis in this animal model for multiple sclerosis (MS) involves early microglial activation, but no infiltration of T‐lymphocytes. Therefore, this model could mimic early stages of oligodendrocyte degeneration Affected oligodendrocytes express the common neurotrophin receptor, p75NTR, a ‘stress‐receptor’ which under certain circumstances can induce apoptosis. Only affected oligodendrocytes in MS lesions and MS animal models express this receptor. In order to study the significance of p75NTR in the fate of oligodendrocytes, we have exposed wild‐type as well as p75NTR‐knockout mice to a 0.2% (w/w) cuprizone diet and performed a comparative immunohistochemical analysis of the corpus callosum at various time points. Surprisingly, our results show that the absence of p75NTR did not alter cuprizone‐induced oligodendrocyte death (and subsequent de‐ or remyelination). Apparently, intracellular apoptosis pathways in adult oligodendrocytes do not require p75NTR activated signal transduction in the absence of T‐lymphocytes and T‐lymphocyte derived cytokines.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biological and medical sciences</subject><subject>central nervous system</subject><subject>corpus callosum</subject><subject>Corpus Callosum - pathology</subject><subject>Cuprizone</subject><subject>Demyelinating Diseases - chemically induced</subject><subject>Demyelinating Diseases - pathology</subject><subject>Demyelinating Diseases - physiopathology</subject><subject>Human viral diseases</subject><subject>immunohistochemistry</subject><subject>Infectious diseases</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Monoamine Oxidase Inhibitors</subject><subject>multiple sclerosis</subject><subject>Nerve Regeneration</subject><subject>Neurology</subject><subject>neurotrophin receptor</subject><subject>oligodendrocyte</subject><subject>Oligodendroglia - pathology</subject><subject>Receptor, Nerve Growth Factor - genetics</subject><subject>T-Lymphocytes - pathology</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Viral diseases</subject><subject>Viral diseases of the lymphoid tissue and the blood. Aids</subject><issn>0305-1846</issn><issn>1365-2990</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkFtLwzAYhoMobh7-gvTGy3Zf2uYE3ujQ6ZgTRFH0IiRpqpldO9oON3-9qdOZi-SD93lD8iAUYIiwX4NZhBNKwlgIiGIAEgFQQqPVDupvg13UhwRIiHlKe-igaWbgSUbFPuphGnMsgPfR64KR6cN94MrMLqzfyjaoCvdW-SmrK7NubZBZ1b57IjDLRe2-qtKGHl8am_lovraFK1XrqrJDhoRdTAY0mDtjj9BerorGHv-eh-jx6vJheB1O7kY3w_NJ6OIU0zCBVOVAjBbEmJwkjGVCC6yNJhpIznWageYkjjUFEefM5CA0x2CFMTzFaXKITjb3LpZ6bjPpHzlX9Vr-_dIDp7-Aaowq8lqVxjX_HIsT7lV57mzDfbrCrv9zkJ11OZOdXNnJlZ11-WNdruT0fOoHXw83dde0drWtq_pDUpYwIp-mI3k7eh6_jBmXw-QbQmSDug</recordid><startdate>200512</startdate><enddate>200512</enddate><creator>Copray, J. C. V. M.</creator><creator>Küst, B. M.</creator><creator>Mantingh-Otter, I.</creator><creator>Boddeke, H. W. G. M.</creator><general>Blackwell Science Ltd</general><general>Blackwell Science</general><scope>BSCLL</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope></search><sort><creationdate>200512</creationdate><title>p75NTR independent oligodendrocyte death in cuprizone-induced demyelination in C57BL/6 mice</title><author>Copray, J. C. V. M. ; Küst, B. M. ; Mantingh-Otter, I. ; Boddeke, H. W. G. M.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i2416-304af05cb95ccf5377d9b91bcb5b05f8b4d0b8522b6092f7cf09b810e9cc84143</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biological and medical sciences</topic><topic>central nervous system</topic><topic>corpus callosum</topic><topic>Corpus Callosum - pathology</topic><topic>Cuprizone</topic><topic>Demyelinating Diseases - chemically induced</topic><topic>Demyelinating Diseases - pathology</topic><topic>Demyelinating Diseases - physiopathology</topic><topic>Human viral diseases</topic><topic>immunohistochemistry</topic><topic>Infectious diseases</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Monoamine Oxidase Inhibitors</topic><topic>multiple sclerosis</topic><topic>Nerve Regeneration</topic><topic>Neurology</topic><topic>neurotrophin receptor</topic><topic>oligodendrocyte</topic><topic>Oligodendroglia - pathology</topic><topic>Receptor, Nerve Growth Factor - genetics</topic><topic>T-Lymphocytes - pathology</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Viral diseases</topic><topic>Viral diseases of the lymphoid tissue and the blood. Aids</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Copray, J. C. V. M.</creatorcontrib><creatorcontrib>Küst, B. M.</creatorcontrib><creatorcontrib>Mantingh-Otter, I.</creatorcontrib><creatorcontrib>Boddeke, H. W. G. M.</creatorcontrib><collection>Istex</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><jtitle>Neuropathology and applied neurobiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Copray, J. C. V. M.</au><au>Küst, B. M.</au><au>Mantingh-Otter, I.</au><au>Boddeke, H. W. G. M.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>p75NTR independent oligodendrocyte death in cuprizone-induced demyelination in C57BL/6 mice</atitle><jtitle>Neuropathology and applied neurobiology</jtitle><addtitle>Neuropathol Appl Neurobiol</addtitle><date>2005-12</date><risdate>2005</risdate><volume>31</volume><issue>6</issue><spage>600</spage><epage>609</epage><pages>600-609</pages><issn>0305-1846</issn><eissn>1365-2990</eissn><coden>NANEDL</coden><abstract>Feeding C57Bl/6 J mice the copper chelator cuprizone leads to selective apoptosis of mature oligodendrocytes and concomitant demyelination predominantly in the corpus callosum. The process of oligodendrocyte apoptosis in this animal model for multiple sclerosis (MS) involves early microglial activation, but no infiltration of T‐lymphocytes. Therefore, this model could mimic early stages of oligodendrocyte degeneration Affected oligodendrocytes express the common neurotrophin receptor, p75NTR, a ‘stress‐receptor’ which under certain circumstances can induce apoptosis. Only affected oligodendrocytes in MS lesions and MS animal models express this receptor. In order to study the significance of p75NTR in the fate of oligodendrocytes, we have exposed wild‐type as well as p75NTR‐knockout mice to a 0.2% (w/w) cuprizone diet and performed a comparative immunohistochemical analysis of the corpus callosum at various time points. Surprisingly, our results show that the absence of p75NTR did not alter cuprizone‐induced oligodendrocyte death (and subsequent de‐ or remyelination). Apparently, intracellular apoptosis pathways in adult oligodendrocytes do not require p75NTR activated signal transduction in the absence of T‐lymphocytes and T‐lymphocyte derived cytokines.</abstract><cop>Oxford, UK</cop><pub>Blackwell Science Ltd</pub><pmid>16281908</pmid><doi>10.1111/j.1365-2990.2005.00656.x</doi><tpages>10</tpages></addata></record> |
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subjects | Animals Apoptosis Biological and medical sciences central nervous system corpus callosum Corpus Callosum - pathology Cuprizone Demyelinating Diseases - chemically induced Demyelinating Diseases - pathology Demyelinating Diseases - physiopathology Human viral diseases immunohistochemistry Infectious diseases Injuries of the nervous system and the skull. Diseases due to physical agents Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Monoamine Oxidase Inhibitors multiple sclerosis Nerve Regeneration Neurology neurotrophin receptor oligodendrocyte Oligodendroglia - pathology Receptor, Nerve Growth Factor - genetics T-Lymphocytes - pathology Traumas. Diseases due to physical agents Viral diseases Viral diseases of the lymphoid tissue and the blood. Aids |
title | p75NTR independent oligodendrocyte death in cuprizone-induced demyelination in C57BL/6 mice |
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