Inflammatory glia mediate delayed neuronal damage after ischemia in the central nervous system.
Reactive microglia respond within hours to central nervous system ischemic injury as exhibited by increased surface molecules, including the scavenger receptor. It is at least several days after an insult, however, before these activated mononuclear phagocytes reach a peak of secretory activity with the release of neurotoxins. This period of cytotoxin secretion is associated with a delayed neuronal loss seen in tissues neighboring sites of ischemia. Microglia-suppressing drugs reduce tissue production of neurotoxic factors and improve functional outcome after ischemic injury. Immunosuppressive therapy may offer a means to reduce late neuronal damage associated with stroke.
Giulian
D
D
Department of Neurology, Baylor College of Medicine, Houston, TX 77030.
Vaca
K
K
D000818:Animals; D002490:Central Nervous System / Q000098:blood supply*; D002493:Central Nervous System Diseases / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D007249:Inflammation / Q000209:etiology / Q000473:pathology / Q000503:physiopathology; D007511:Ischemia / Q000150:complications / Q000378:metabolism / Q000473:pathology*; D017628:Microglia / Q000378:metabolism / Q000502:physiology*; D009474:Neurons / Q000473:pathology*; D009498:Neurotoxins / Q000378:metabolism; D010586:Phagocytes / Q000378:metabolism; D011817:Rabbits; D051381:Rats; D013997:Time Factors
D009498:Neurotoxins