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Excitotoxic and apoptotic neuronal death induce different patterns of glial activation in vitro
Author(s) -
PérezCapote Kamil,
Serratosa Joan,
Solà Carme
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.03183.x
Subject(s) - programmed cell death , apoptosis , neuroglia , microglia , biology , glutamate receptor , microbiology and biotechnology , nitric oxide , astrocyte , phagocytosis , neuroscience , necrosis , neurodegeneration , immunology , inflammation , pathology , central nervous system , medicine , biochemistry , endocrinology , receptor , genetics , disease
We have studied glial activation in rat cerebellar neuronal‐glial cultures after inducing neuronal death using various stimuli. Cultures were exposed to 100 µ m glutamate for 20 min, which induces excitotoxic neuronal death, or to potassium/serum deprivation, which induces apoptosis of granule neurons. We evaluated alterations in several parameters related to glial activation: nuclear factor‐κB activation, nitric oxide and tumour necrosis factor‐α production, which are associated with a pro‐inflammatory response, glial proliferation and phagocytic activity. Although the two experimental models of neuronal damage resulted in the death of most neuronal cells within 24 h, differences were observed in the response of the various glial parameters evaluated. While nitric oxide production was not detected in any case, tumour necrosis factor‐α production, nuclear factor‐κB activation and glial proliferation were only induced in the presence of excitotoxic neuronal death. However, phagocytosis was induced in both cases, although earlier in the case of apoptotic neuronal death. These results show that glial cells respond to excitotoxic neuronal death with an inflammatory response associated with proliferation and phagocytosis. In contrast, whilst glial cells do not produce pro‐inflammatory molecules in the presence of apoptotic neuronal death, phagocytic activity is rapidly induced.