Dephosphorelation of Bad and upregulation of Bcl-2 in hippocampus of rats following limbic seizure induced by kainic acid injection into amygdaloid nucleus.
- Author:
Tian-Fu LI
1
;
Chuan-Zhen LU
;
Zuo-Li XIA
;
Jing-Zhong NIU
;
Ming-Feng YANG
;
Yu-Min LUO
;
Zhen HONG
Author Information
1. Department of Neurology, Affiliated Hospital of Taishan Medical College, Taian 271000, China. tianfuli88@hotmail.com
- Publication Type:Journal Article
- MeSH:
Amygdala;
physiology;
Animals;
Epilepsies, Partial;
chemically induced;
metabolism;
Hippocampus;
metabolism;
Kainic Acid;
Male;
Microinjections;
Phosphorylation;
Proto-Oncogene Proteins c-bcl-2;
biosynthesis;
genetics;
Rats;
Up-Regulation;
bcl-Associated Death Protein;
metabolism
- From:
Acta Physiologica Sinica
2005;57(3):310-318
- CountryChina
- Language:Chinese
-
Abstract:
The purpose of the present study was to explore the seizure-induced changes in Bad (Bcl-2-associated death protein), 14-3-3, phosphoBad, Bcl-2 and Bcl-XL expression in the rat model of focal limbic seizure. Unilateral intra-amygdaloid injection of kainic acid (KA) was made to induce seizure. Electroencephalogram (EEG) and regional cerebral flow (r-CBF) were monitored continuously. Diazepam (30 mg/kg) was administered to terminate the seizure. The apoptotic and surviving neurons in the hippocampus were observed by terminal deoxynucleotidyl transferrase-mediated dUTP nick end labeling (TUNEL) and cresyl violet staining, the expression of Bad, 14-3-3, phosphoBad, Bcl-2 and Bcl-XL were detected with immunofluorescence, Western blot and immunoprecipitation. The results showed that TUNEL-positive neurons appeared at 8 h and reached maximum at 24 h following seizure cessation within the ipsilateral CA3 subfield of the hippocampus. Seizure induced the dephosphorylation of Bad and the dissociation of Bad from its chaperone protein 14-3-3 and subsequent dimerization of Bad with Bcl-XL. The expression of phosphoBad decreased and Bcl-2 increased. There was little change in r-CBF after the seizure. These results suggest that seizure leads to a dephosphorylation of Bad and an upregulation of Bcl-2. Dephosphorylation of Bad may be injurious while the upregulation of Bcl-2 may be protective to the brain damage induced by seizures, but not related with r-CBF.
