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Reactive gliosis of immature Bergmann glia and microglial cell activation in response to cell death of granule cell precursors induced by methylazoxymethanol treatment in developing rat cerebellum.

Abstract

The morphology, organization and expression of proliferating cell nuclear antigen (PCNA) and the cytoskeletal proteins vimentin and GFAP in immature Bergmann glial cells were studied after a developmental injury induced by a single dose of the cytotoxic agent methylazoxymethanol (MAM) administered on postnatal day 5. This drug, which produces cell death of cerebellar granule cell precursors, did not induce apoptosis in Bergmann glial cells, which are in a proliferative stage. After MAM treatment, PCNA staining showed a severe depletion of PCNA-positive granule cell precursors, whereas PCNA-positive Bergmann glial nuclei in the Purkinje cell layer were preserved. Moreover, the quantitative analysis revealed an increase in the density of both Purkinje cells and PCNA-positive Bergmann glial cells per mm of Purkinje cell layer in MAM-treated rats relative to age-matched controls, but the numerical ratio between these two cell populations remains invariable after MAM treatment. Vimentin and GFAP immunocytochemistry revealed a reinforcement of the Bergmann glial palisade with overexpression of both proteins and thicker immunoreactive glial processes in MAM-treated rats. At the ultrastructural level, Bergmann glial processes closely associated with dying cells in different stages of apoptosis were observed. Frequently, these processes enclosed dying cells in extracellular compartments. Furthermore, phagosomes containing apoptotic bodies were found in Bergmann fibers of MAM-treated rats. These data indicate that the cell death of granule cell precursors triggers a reactive response in immature Bergmann glia. We suggest that this response reflects the plasticity of Bergmann glia to control the neuronal microenvironment in the maturing molecular layer, protecting healthy cells against the potentially harmful contents of dying cells. In situ labeling of cell death with the TUNEL method revealed that the cell death of granule cell precursors is of the apoptotic type. The participation of ameboid microglial cells in the phagocytosis of apoptotic cells was shown with tomato lectin histochemistry and ultrastructural analysis. Moreover, the presence of mitosis in this microglial population demonstrates its proliferative activity in regions of extensive cell death.

Authors+Show Affiliations

,

Departamento de Anatomía y Biología Celular, Facultad de Medicina, Santander, Spain. lafargam@medi-unican.es

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Source

Anatomy and embryology 198:2 1998 Aug pg 111-22

MeSH

Animals
Apoptosis
Cerebellar Cortex
Fluorescent Antibody Technique, Direct
Glial Fibrillary Acidic Protein
Gliosis
In Situ Nick-End Labeling
Lectins
Male
Methylazoxymethanol Acetate
Microglia
Mitosis
Neurons
Proliferating Cell Nuclear Antigen
Rats
Rats, Sprague-Dawley
Stem Cells
Vimentin

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9725770

Citation

Lafarga, M, et al. "Reactive Gliosis of Immature Bergmann Glia and Microglial Cell Activation in Response to Cell Death of Granule Cell Precursors Induced By Methylazoxymethanol Treatment in Developing Rat Cerebellum." Anatomy and Embryology, vol. 198, no. 2, 1998, pp. 111-22.
Lafarga M, Andres MA, Calle E, et al. Reactive gliosis of immature Bergmann glia and microglial cell activation in response to cell death of granule cell precursors induced by methylazoxymethanol treatment in developing rat cerebellum. Anat Embryol. 1998;198(2):111-22.
Lafarga, M., Andres, M. A., Calle, E., & Berciano, M. T. (1998). Reactive gliosis of immature Bergmann glia and microglial cell activation in response to cell death of granule cell precursors induced by methylazoxymethanol treatment in developing rat cerebellum. Anatomy and Embryology, 198(2), pp. 111-22.
Lafarga M, et al. Reactive Gliosis of Immature Bergmann Glia and Microglial Cell Activation in Response to Cell Death of Granule Cell Precursors Induced By Methylazoxymethanol Treatment in Developing Rat Cerebellum. Anat Embryol. 1998;198(2):111-22. PubMed PMID: 9725770.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reactive gliosis of immature Bergmann glia and microglial cell activation in response to cell death of granule cell precursors induced by methylazoxymethanol treatment in developing rat cerebellum. AU - Lafarga,M, AU - Andres,M A, AU - Calle,E, AU - Berciano,M T, PY - 1998/9/2/pubmed PY - 1998/9/2/medline PY - 1998/9/2/entrez SP - 111 EP - 22 JF - Anatomy and embryology JO - Anat. Embryol. VL - 198 IS - 2 N2 - The morphology, organization and expression of proliferating cell nuclear antigen (PCNA) and the cytoskeletal proteins vimentin and GFAP in immature Bergmann glial cells were studied after a developmental injury induced by a single dose of the cytotoxic agent methylazoxymethanol (MAM) administered on postnatal day 5. This drug, which produces cell death of cerebellar granule cell precursors, did not induce apoptosis in Bergmann glial cells, which are in a proliferative stage. After MAM treatment, PCNA staining showed a severe depletion of PCNA-positive granule cell precursors, whereas PCNA-positive Bergmann glial nuclei in the Purkinje cell layer were preserved. Moreover, the quantitative analysis revealed an increase in the density of both Purkinje cells and PCNA-positive Bergmann glial cells per mm of Purkinje cell layer in MAM-treated rats relative to age-matched controls, but the numerical ratio between these two cell populations remains invariable after MAM treatment. Vimentin and GFAP immunocytochemistry revealed a reinforcement of the Bergmann glial palisade with overexpression of both proteins and thicker immunoreactive glial processes in MAM-treated rats. At the ultrastructural level, Bergmann glial processes closely associated with dying cells in different stages of apoptosis were observed. Frequently, these processes enclosed dying cells in extracellular compartments. Furthermore, phagosomes containing apoptotic bodies were found in Bergmann fibers of MAM-treated rats. These data indicate that the cell death of granule cell precursors triggers a reactive response in immature Bergmann glia. We suggest that this response reflects the plasticity of Bergmann glia to control the neuronal microenvironment in the maturing molecular layer, protecting healthy cells against the potentially harmful contents of dying cells. In situ labeling of cell death with the TUNEL method revealed that the cell death of granule cell precursors is of the apoptotic type. The participation of ameboid microglial cells in the phagocytosis of apoptotic cells was shown with tomato lectin histochemistry and ultrastructural analysis. Moreover, the presence of mitosis in this microglial population demonstrates its proliferative activity in regions of extensive cell death. SN - 0340-2061 UR - https://www.unboundmedicine.com/medline/citation/9725770/Reactive_gliosis_of_immature_Bergmann_glia_and_microglial_cell_activation_in_response_to_cell_death_of_granule_cell_precursors_induced_by_methylazoxymethanol_treatment_in_developing_rat_cerebellum_ DB - PRIME DP - Unbound Medicine ER -