Characterization of microglial reaction after middle cerebral artery occlusion in rat brain.
We have studied the microglial reaction that accompanies cortical infarction induced by middle cerebral artery occlusion (MCAO). Lectin histochemistry with the B4-isolectin from Griffonia simplicifolia as well as immunocytochemistry with a panel of monoclonal antibodies directed against major histocompatibility complex (MHC) and lymphocytic antigens were performed. Principal attention was focused on neocortical and thalamic regions, representative of primary and secondary ischemic damage, respectively. With the lectin procedure, activated microglial cells were abundant in the neocortex 24 hours after MCAO. In contrast, microglial activation in the thalamus was not apparent until day 2 after MCAO. On day 5, MHC class II antigen was expressed by reactive microglia in fiber tracts traversing the striatum, but was absent from activated microglia in the primary cortical infarction area. MHC class I and lymphocytic antigens were expressed differentially on microglia with class I antigens appearing early and lymphocytic antigens appearing late in the time course after focal ischemia. The findings are compatible with previous studies during global ischemia and confirm the early activation and the progressive nature of immunomolecule expression on activated microglia after an ischemic insult. In addition to neocortical and thalamic sites, our results showed an early microglial activation to be present also in forebrain regions outside of the middle cerebral artery (MCA) territory, such as the contralateral cortex and hippocampus. A unilateral microglial reaction was also detectable after long-term survival (> or = 4 weeks) in the pyramidal tracts, as well as in the corticospinal tracts at cervical but not lumbar spinal cord levels. Ischemia-induced neuronal damage, as evaluated by Nissl staining, was found only in cortical and thalamic regions. We conclude that the demonstration of reactive microglia indicates not only imminent ischemic neuronal damage within MCA territory but can also delineate extra-focal disturbances, possibly reflecting subtle and transitory changes in neuronal activity.
Morioka
T
T
Department of Neurological Surgery, University of Florida, Gainesville 32610-0244.
Kalehua
A N
AN
Streit
W J
WJ
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications*; D002539:Cerebral Arterial Diseases / Q000150:complications*; D002544:Cerebral Infarction / Q000209:etiology / Q000473:pathology*; D005911:Gliosis / Q000209:etiology / Q000473:pathology*; D016130:Immunophenotyping; D007249:Inflammation; D008214:Lymphocytes / Q000473:pathology; D009457:Neuroglia / Q000473:pathology*; D051381:Rats; D017208:Rats, Wistar