Microglial response to transient focal cerebral ischemia: an immunocytochemical study on the rat cerebral cortex using anti-phosphotyrosine antibody.
Microglial response to transient focal ischemia was examined using an immunohistochemical method with a monoclonal antibody to phosphotyrosine (P-Tyr). For this purpose, a rat model of reversible middle cerebral artery occlusion for 1 h was used. Compared with results in the noninsulted hemisphere, there was a significant increase in P-Tyr immunolabeling of the microglia in the insulted cerebral cortex 3 h postreperfusion. This microglial reaction progressed up to 24 h after ischemic insult. In the affected cerebral cortex, morphological changes of the microglial positive for P-Tyr were also observed, with shortened and thickened processes, enlarged cell bodies, and ameboid features. Cell density analysis did not show any apparent change in number of P-Tyr-positive microglia in the insulted cortex at 6, 12, and 24 h after reperfusion, suggesting that the cells with increased P-Tyr immunoreactivity were resident microglia. The present findings suggest that signal transduction mediated by tyrosine phosphorylation is involved in the microglial response to ischemic injury in the rat cerebral cortex.
Korematsu
K
K
Department of Neurosurgery, Kumamoto University Medical School, Japan.
Goto
S
S
Nagahiro
S
S
Ushio
Y
Y
D000818:Animals; D000911:Antibodies, Monoclonal; D002452:Cell Count; D002540:Cerebral Cortex / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D002546:Ischemic Attack, Transient / Q000378:metabolism* / Q000473:pathology; D008297:Male; D017628:Microglia / Q000378:metabolism*; D019000:Phosphotyrosine; D051381:Rats; D017208:Rats, Wistar; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000276:immunology / Q000378:metabolism
D000911:Antibodies, Monoclonal; D019000:Phosphotyrosine; D014443:Tyrosine