Activation of Ca2+-dependent K+ Channels Is Essential for Bradykinin-induced Microglial Migration
نویسندگان
چکیده
Bradykinin (BK) is produced and acts at the site of injury and inflammation not only in periphery but also in the brain. In the central nervous system, migration of microglia towards damaged tissue plays a role in regeneration under pathological condition. In the present study, we found that bradykinin (BK) induced migration of cultured microglia, which was blocked by charybdotoxin, a blocker of large conductance Ca-dependent K channels, but not by pertussis toxin (PTX). These results indicate that activation of large conductance Ca2+-activated K+ channel is required for BK-induced microglial migration, while activation of PTX-sensitive G protein is not. Our findings may help to understand the function of kinins in the brain and the role of microglia in response to brain injury.
منابع مشابه
Bradykinin-induced microglial migration mediated by B1-bradykinin receptors depends on Ca2+ influx via reverse-mode activity of the Na+/Ca2+ exchanger.
Bradykinin (BK) is produced and acts at the site of injury and inflammation. In the CNS, migration of microglia toward the lesion site plays an important role pathologically. In the present study, we investigated the effect of BK on microglial migration. Increased motility of cultured microglia was mimicked by B1 receptor agonists and markedly inhibited by a B1 antagonist but not by a B2 recept...
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