Activation of JNK and p38 in rat hippocampus after kainic acid induced seizure.
- Author:
Song Hee JEON
1
;
Yong Sik KIM
;
Chang Dae BAE
;
Joo Bae PARK
Author Information
1. Department of Molecular Cell Biology and Samsung Biomedical Research Institute, Sunkyunkwan University School of Medicine, Suwon, Korea.
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
hippocampus;
kainic acid;
ERK;
JNK;
p38;
phosphorylation
- MeSH:
Animal;
Enzyme Activation;
Hippocampus/*drug effects/enzymology;
Kainic Acid/*pharmacology;
Limbic System/drug effects;
Male;
Mitogen-Activated Protein Kinases/*metabolism;
Rats;
Seizures/*chemically induced
- From:Experimental & Molecular Medicine
2000;32(4):227-230
- CountryRepublic of Korea
- Language:English
-
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.
