Abstract
Kainic acid, an analogue of glutamate, causes limbic seizures and induces cell death in the rat brain. We examined the activation of MAPK family kinases; ERKs, JNKs and p38 kinase in rat hippocampus after KA treatment. Activation of all three kinases were observed at 30 min after the treatment, but, in contrary to ERK phosphorylation, which lasted up to 3 h, the phosphorylation of JNK and p38 returned to the basal level by 2 h. The phosphorylation of' upstream kinases for the MAPK family was distinct. The phosphorylation of MEK1 clearly increased at 30 min but diminished rapidly thereafter. The phosphorylation of MKK6 was also increased but reached peak at 2 h after KA treatment. However, the phosphorylation of other upstream kinases, SEK1 and MKK3, gradually decreased to 3 h after KA treatment. These results indicate that the KA activates all of the three MAPK family kinases with different time patterns and suggest the possibility that MKK3 and MKK6, and SEK1 may not be the upstream kinases for p38 and JNK in rat hippocampus.
Highlights
Glutamate has been known to play crucial roles in synaptic plasticity (Nicoll et al, 1988) and excitotoxic cell death (Choi, 1988)
P54 c-Jun N-terminal kinase (JNK) was expressed in hippocampus, the phosphorylation of p54 JNK was hardly detectable in rat hippocampus
We showed that the other members of mitogen-activated protein kinase (MAPK) family, JNK and p38, were activated in rat hippocampus after kainic acid (KA) treatment
Summary
Glutamate has been known to play crucial roles in synaptic plasticity (Nicoll et al, 1988) and excitotoxic cell death (Choi, 1988). We have been studying the induction of immediate early genes such as c-fos and c-jun and activation of MAPK family kinases after electrically-induced seizures. Various glutamates are known to activate MAPKs in cell lines. The role of these glutamate receptors in the activation of MAPKs in rat brain after electrically-induced seizures are not clearly understood. KA is known to induce the expression of various immediate early genes such as c-fos and c-jun and activates signaling molecules in rat brain. The KA-induced signal transduction pathway leading to the induction of immediate early gene expression and excitotoxic cell death are largely unknown in vivo
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