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학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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Background : After the ischemic insult of the brain, the level of excitotoxic amino acids rapidly increases, which is followed by and expression of various cytokine/chemokines from brain cells. These series of events appear to be related to the pathogenesis of neuronal cell death in the ischemic brain. However, whether an activation of glutamate receptors induces cytokine expression in astrocytes/microglia has not yet been sufficiently studied. Methods : Astrocytes and microglia were cultured from young rat brain. These cells were stimulated for 24 hours by glutamate (1mM), NMDA (100 uM), quisqualate (100uM), ACPD (50 uM)., kainate (100 uM),AMPA (20 uM), IL-1b (200 u/ml), IL-6 (100 ng/ml) and LPS (1 ug/ml). Using immunocytochemical methods, the immunoreactivity of following proteins were studied: IL-1b, IL-6, TGF b, MCP-1 and MIP. Results : Quisqualate and ACPD stimuli induced immunoreactivity of IL-1b, IL-6, TGF b in astrocytes while glutamate, NMDA, LPS, IL-1b and IL-6 did not. Quisqualate and ACPD also induced immunoreactivity of MCP but not that of MIP in astrocytes. LPS, IL-6, TGF b and TNF a induced expression of MCP-1 but not MIP. In the cultured microglia, none of the above stimuli induced expression of cytokines. Conclusion : Activation of certain glutamate receptors may stimulate the astrocytes to produce various cytokines and chemokines. Activation of glutamate receptors in early ischemic brain may be one of the factors inducing cytokine/chemokine cascades occurring in theischemic brain. Korean Journal of Stroke 1999;1(2): 240~245
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