ACTIVATION OF P38(MAPK) IN MICROGLIA AFTER ISCHEMIA

p38(MAPK) has been implicated in the regulation of proinflammatory cyt okines and apoptosis in vitro. To understand its role in neurodegenera tion, we determined the lime course and localization of the dually pho sphorylated active form of p38(MAPK) in hippocampus after global foreb rain ischemia, Phosphorylated p38(MAPK) and mitogen-activated protein kinase-activated protein 2 activity increased over 4 days after ischem ia. Phosphorylated p38(MAPK) immunoreactivity was observed in microgli a in regions adjacent to, but not in, the dying CA1 neurons. In contra st, neither c-Jun N-terminal kinase 1 nor p42/p44(MAPK) activity was a ltered after ischemia. These results provide the first evidence for lo calization oi activated p38(MAPK) in the CNS and support a role for p3 8(MAPK) in the microglial response to stress.