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Reactive microglia in dysmyelination and demyelination
Author(s) -
Zhang SuChun,
Goetz Brian D.,
Carré JeanLuc,
Duncan Ian D.
Publication year - 2001
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.1045
Subject(s) - microglia , myelin , biology , neuroglia , oligodendrocyte , pathology , nitric oxide synthase , microbiology and biotechnology , neuroscience , immunology , central nervous system , nitric oxide , inflammation , medicine , endocrinology
The relationship between microglial activation and dysmyelination/demyelination was analyzed in a long‐lived myelin mutant, the Long Evans shaker ( les ) rat, which exhibits early dysmyelination and a later loss of abnormal myelin sheaths. A microglial reaction characterized by progressive morphological transformation and increasing cell density was localized exclusively to white matter during postnatal 2–4 weeks, suggesting a microglial response to dysmyelination and oligodendroglial pathology. A further microglial reaction as marked by microglial expression of MHC II and a concomitant expression in the brain and spinal cord of mRNA for interleukin‐1β (IL‐1β), tumor necrosis factor‐α (TNF‐α), and inducible nitric oxide synthase (iNOS) began around 4 weeks when the remaining myelin was lost. Ultrastructurally, activated microglia ingested numerous myelin figures, suggestive of active phagocytosis. Thus, this study indicates that microglial reaction is graded in chronic neurological disorders and suggests that MHC II expression marks a functional change of activated microglia. GLIA 34:101–109, 2001. © 2001 Wiley‐Liss, Inc.