Microglia as a unique cellular target in the treatment of stroke: potential neurotoxic mediators produced by activated microglia.
The sequalae evoked by an initial ischemic event in the CNS are incredibly complex and involve a wide range of short-term and long-term metabolic adaptations. With regard to the 'penumbra' area, in which cell death occurs over a 1 to 3 day period, defining the roles of potential neurotoxic mediators is crucial. In this regard, upon cellular activation after an ischemic episode, microglia, the resident macrophages of the CNS, can produce large quantities of a number of neurotoxic mediators. These factors include excitatory amino acids, proteases, cytokinases and nitric oxides. In this manuscript, these mediators are reviewed with regard to the potential utility of suppression of microglial function, via immunosuppressive agents, in the treatment of stroke.
D002450:Cell Communication / Q000187:drug effects; D016923:Cell Death / Q000187:drug effects; D002561:Cerebrovascular Disorders / Q000188:drug therapy* / Q000276:immunology; D016207:Cytokines / Q000378:metabolism; D010450:Endopeptidases / Q000378:metabolism; D018846:Excitatory Amino Acids / Q000378:metabolism; D006801:Humans; D017628:Microglia / Q000187:drug effects* / Q000276:immunology / Q000378:metabolism; D009474:Neurons / Q000187:drug effects* / Q000473:pathology
D016207:Cytokines; D018846:Excitatory Amino Acids; D010450:Endopeptidases