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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Veröffentlicht in:Neuropathology and applied neurobiology 2005-12, Vol.31 (6), p.600-609
Hauptverfasser: Copray, J. C. V. M., Küst, B. M., Mantingh-Otter, I., Boddeke, H. W. G. M.
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container_title Neuropathology and applied neurobiology
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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.
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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). 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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. 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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. 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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. 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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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