Mitogen-activated protein kinases phosphorylation in posttraumatic selective vulnerability in rats

Mitogenic stimulation of the Mitogen-activated protein kinase (MAPK) pathway modulates the activity of many transcriptional factors leading to biological responses. Of these, three MAPK cascades are well characterized as extracellular signal-regulated protein kinase (ERK), c-Jun NH(2)-terminal kinase (JNK), and p38 pathways. The aim of this study was to investigate the topographic distribution and the role of activated MAPK pathways after fluid percussion injury (FPI) in rats. In the present results, FPI significantly induced ERK- and JNK-phosphorylation, but not p38-phosphorylation in the cortex and hippocampus at the injury site. The immunoreactivity for phospho-ERK was localized in the superficial neuronal layers, dentate hilar neurons, and the damaged CA3 neurons after 30 mins of FPI. Double immunostaining showed that phospho-ERK was prominent in astrocytes 6 hrs after TBI. The current results suggest that MAPK pathways are involved in signal transduction after FPI.