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Time course of glial proliferation and glial apoptosis following excitotoxic CNS injury.

Abstract

Activation of microglial cells and astrocytes after CNS injury results in changes in their morphology, immunophenotype and proliferative activity and has neurotrophic as well as neurotoxic consequences. However, little is known about the exact time course of glial activation as regards their proliferative activity and their fate. In this study, quantification of the densities of proliferating and non-proliferating microglial cells and astrocytes was carried out over 30 days by counting differentially labeled cells in the striatum and substantia nigra pars reticulata (SNr) after injection of quinolinic acid into the rat striatum. The TdT-mediated dUTP nick end labeling (TUNEL)-reaction was used to detect possible apoptotic mechanisms which limit the glial reaction. At 1 day post injection (p.i.) non-proliferating ameboid microglia/macrophages were seen in the striatum, but at 3 and 5 days p.i. many proliferating, ameboid microglia/macrophages and hypertrophic microglia were detected. At 10 days p.i., the time point with the highest density of hypertrophic microglia, TUNEL-positive microglial cells were observed indicating that apoptotic processes play a role in restricting this reaction. In contrast to this, at early time points, a reduction in the density and glial fibrillary acidic protein (GFAP)-immunoreactivity of astrocytes in the striatum was detected. At later time points, a dense astrogliosis with proliferating astrocytes developed in the dorsal and medial striatum. At 30 days p.i., in the entire striatum a dense astrogliosis was detected. The SNr showed a short period of microglial activation and proliferation and a long lasting astrogliosis without proliferation

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  • Authors+Show Affiliations

    ,

    Department of Neurology, RWTH Aachen, Pauwelsstr. 30, D-52057, Aachen, Germany. marcel.dihne@post.rwth-aachen.de

    , ,

    Source

    Brain research 902:2 2001 Jun 01 pg 178-89

    MeSH

    Animals
    Apoptosis
    Astrocytes
    Brain Injuries
    Cell Count
    Cell Division
    Glial Fibrillary Acidic Protein
    Gliosis
    Immunohistochemistry
    In Situ Nick-End Labeling
    Lectins
    Male
    Microglia
    Neostriatum
    Neurotoxins
    Plant Lectins
    Proliferating Cell Nuclear Antigen
    Quinolinic Acid
    Rats
    Rats, Wistar
    Substantia Nigra
    Time Factors

    Pub Type(s)

    Journal Article

    Language

    eng

    PubMed ID

    11384611

    Citation

    Dihné, M, et al. "Time Course of Glial Proliferation and Glial Apoptosis Following Excitotoxic CNS Injury." Brain Research, vol. 902, no. 2, 2001, pp. 178-89.
    Dihné M, Block F, Korr H, et al. Time course of glial proliferation and glial apoptosis following excitotoxic CNS injury. Brain Res. 2001;902(2):178-89.
    Dihné, M., Block, F., Korr, H., & Töpper, R. (2001). Time course of glial proliferation and glial apoptosis following excitotoxic CNS injury. Brain Research, 902(2), pp. 178-89.
    Dihné M, et al. Time Course of Glial Proliferation and Glial Apoptosis Following Excitotoxic CNS Injury. Brain Res. 2001 Jun 1;902(2):178-89. PubMed PMID: 11384611.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Time course of glial proliferation and glial apoptosis following excitotoxic CNS injury. AU - Dihné,M, AU - Block,F, AU - Korr,H, AU - Töpper,R, PY - 2001/6/1/pubmed PY - 2001/8/10/medline PY - 2001/6/1/entrez SP - 178 EP - 89 JF - Brain research JO - Brain Res. VL - 902 IS - 2 N2 - Activation of microglial cells and astrocytes after CNS injury results in changes in their morphology, immunophenotype and proliferative activity and has neurotrophic as well as neurotoxic consequences. However, little is known about the exact time course of glial activation as regards their proliferative activity and their fate. In this study, quantification of the densities of proliferating and non-proliferating microglial cells and astrocytes was carried out over 30 days by counting differentially labeled cells in the striatum and substantia nigra pars reticulata (SNr) after injection of quinolinic acid into the rat striatum. The TdT-mediated dUTP nick end labeling (TUNEL)-reaction was used to detect possible apoptotic mechanisms which limit the glial reaction. At 1 day post injection (p.i.) non-proliferating ameboid microglia/macrophages were seen in the striatum, but at 3 and 5 days p.i. many proliferating, ameboid microglia/macrophages and hypertrophic microglia were detected. At 10 days p.i., the time point with the highest density of hypertrophic microglia, TUNEL-positive microglial cells were observed indicating that apoptotic processes play a role in restricting this reaction. In contrast to this, at early time points, a reduction in the density and glial fibrillary acidic protein (GFAP)-immunoreactivity of astrocytes in the striatum was detected. At later time points, a dense astrogliosis with proliferating astrocytes developed in the dorsal and medial striatum. At 30 days p.i., in the entire striatum a dense astrogliosis was detected. The SNr showed a short period of microglial activation and proliferation and a long lasting astrogliosis without proliferation SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/11384611/Time_course_of_glial_proliferation_and_glial_apoptosis_following_excitotoxic_CNS_injury_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(01)02378-2 DB - PRIME DP - Unbound Medicine ER -