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Response of endogenous glial cells to motor neuron degeneration induced by toxic ricin
Author(s) -
Streit Wolfgang J.,
Kreutzberg Georg W.
Publication year - 1988
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.902680209
Subject(s) - glial fibrillary acidic protein , griffonia simplicifolia , microglia , biology , immunocytochemistry , neuroglia , astrocyte , gfap stain , pathology , axotomy , phagocytosis , microbiology and biotechnology , glial scar , wallerian degeneration , neuroscience , lectin , central nervous system , regeneration (biology) , immunohistochemistry , immunology , endocrinology , medicine , inflammation
The injection of toxic lectin from Ricinus communis into the rat facial nerve resulted in suicide transport and rapid degeneration of facial motor neurons. The reaction of glial cells to neuronal death in comparison with nerve crush lesions was studied by using lectin‐HRP conjugates derived from Griffonia simplicifolia for the selective staining of microglial cells at both light and electron microscopic levels. In addition, the proliferative activity of microglia was assessed by quantification of 3 H‐thymidine incorporation. The astrocytic response was evaluated by light microscopic immunocytochemistry for glial fibrilliary acidic protein. In the degenerating facial nucleus local microglial cells responded by rapid proliferation and phagocytosis of neuronal debris. After nerve crush, no phagocytes were observed, but microglial proliferation and perineuronal satellitosis were prominent. The astrocytic expression of glial fibrillary acidic protein in response to nerve crush proceeded gradually over a period of several weeks after which it declined, contrasting with accelerated astrocytic hypertrophy and permanent glial scarring after neuronal degeneration. These results show that the expression of glial fibrillary acidic protein by fibrous astrocytes is intensified after lethal neuronal injury compared to sublethal insults. In the absence of any observations indicating participation of hematogenous elements, it is proposed that local microglial cells transform into brain macrophages.