Activation of JNK and p38 in rat hippocampus after kainic acid induced seizure

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.

Expression changes in mouse brains following nicotine-induced seizures: the modulation of transcription factor networks

“…Activation of the MAP kinase (MAPK) family following seizure activity was previously described (25,39). Our model of nicotine-induced seizures detected four differentially overexpressed genes, Fos, Nr4a1, Dusp1, and Nfkbia, involved in the MAPK signaling pathway.…”

Status Epilepticus-Induced Somatostatinergic Hilar Interneuron Degeneration Is Regulated by Striatal Enriched Protein Tyrosine Phosphatase

“…Furthermore ERK activation may afford protection against c-Jun N-terminal kinase (JNK)-mediated cell death (Xia et al, 1995). Interestingly, JNK is stimulated by seizure activity in the hippocampus (Jeon et al, 2000), and thus repressed ERK activity may increase the vulnerability of hilar interneurons to excitotoxic cell death via JNK-dependent signaling. In this context, it is interesting to note that somatostatinergic hilar interneurons are highly vulnerable to a number of excitatory insults, including ischemia and trauma, as well as SE (Lowenstein et al, 1992;Matsuyama et al, 1993).…”

Role of γ-aminobutyric acid B (GABAB) receptors in the regulation of kainic acid-induced cell death in mouse hippocampus

“…injection. Several studies reported that the p-ERK was increased by systemic administration of KA in the rat hippocampus (Mielke et al, 1999;Jeon et al, 2000). Recent studies showed that seizures induced the sprouting of mossy fibers in the rat hippocampus CA3 region (e.g.…”

“…KA, administered i.c.v., induced the lesion of CA3 pyramidal neurons in mice (Ferraguti et al, 2001;Lee et al, 2002;Lee et al, 2003). The phosphorylated extracellular signal-regulated kinase (p-ERK) is increased by systemic administration of KA in the rat hippocampus (Mielke et al, 1999;Jeon et al, 2000). Seizures induce the sprouting of mossy fibers in the CA3 region of rat hippocampus (Ben-Ari and Cossart, 2000).…”