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PMID: 7040607 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Changes in expression of glial antigens M1 and C1 after cerebellar injury.

Lagenaur C, Masters C, Schachner M

Abstract

In response to mechanical injury in the adult mouse cerebellum, Bergmann glia and astrocytes of the granular layer exhibit abnormally increased expression of M1 antigen, while expression of C1 antigen in Bergmann glia is reduced. these reciprocal changes in two different astrocytic antigenic determinants (each recognized by monoclonal antibodies) are easily detected in the immediate area of the wound 4 days after the lesion. Although loss of C1 antigen from Bergmann glia remains localized to the area of the wound, abnormal M1 expression becomes widespread in cerebellar astrocytes, also affecting the contralateral side of the injured cerebellum at its peak 8 to 12 days after injury. These findings suggest that previous observations of abnormal expression of the two antigens in the cerebellum of mutant mice (Sommer, I., and M. Schachner (1981) J. Supramol. Struct. 16: 53-74) might be interpreted with the view that a glial reaction to pathological state might be induced by genetically programmed neuronal cell death and/or abnormal development. We therefore postulate that expression of M1 in astrocytes that normally do not express this antigen and repression of C1 in normally positive astrocytes are indicative of a distinct functional state of astroglia, reactive gliosis.

MeSH Terms
Animals Antigens/immunology Astrocytes/immunology Cerebellum/immunology,injuries Fluorescent Antibody Technique Mice Mice, Inbred C57BL Neuroglia/immunology
Chemicals
Antigens
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Lagenaur C
Masters C
Schachner M
Article Info
Journal
The Journal of neuroscience : the official journal of the Society for Neuroscience
Abbr.
J Neurosci
ISSN
0270-6474
Published
1982-04-00
Pages
470-6
Language
English
Region
United States
NLM ID
8102140
PMCID
PMC6564253
Subset
IM
Grants
NINDS NIH HHS · IF32NS06058-01 · United States
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