Changes of AP-1 Binding Activities in Rat Brain by Electroconvulsive Shock.
- Author:
Yeon Ho JOO
1
;
Yong Min AHN
;
Ung Gu KANG
;
Young Jin KOO
;
Yong Sik KIM
Author Information
1. Department of Psychiatry, University of Ulsan College of Medicine, Asan Medical Center, Seoul, Korea.
- Publication Type:Original Article
- Keywords:
ECS (electroconvulsive shock);
IEG (immediate early gene);
AP-1;
NMDAR1 (N-methyl-D-aspartate receptor)
- MeSH:
Animals;
Binding Sites;
Brain*;
Carrier Proteins;
Cerebellum;
Electroshock*;
Hippocampus;
Rats*;
Schizophrenia;
Transcription Factor AP-1*
- From:Journal of Korean Neuropsychiatric Association
2003;42(5):544-552
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVES: ECS could have therapeutic effects on psychiatric illnesses by inducing IEGs, which in turn regulates expression of their target genes. We observed AP-1 binding activity and identified AP-1 binding proteins in NMDAR1, late response gene of IEGs, which considered as the candidate gene for schizophrenia. METHODS: By gel shift assay and supershift assay, we observed binding activities and AP-1 binding proteins in NMDAR1. Because IEGs are induced rapidly but transiently by external stimuli, there is a possibility that the expression of IEGs is negatively feedbacked by their own products via their AP-1 binding sites. For that purpose, we also observed AP-1 binding activity of c-fos and c-jun via gel shift and supershift assay. RESULTS: ECS increased AP-1 binding activities of NMDAR1 gene, contributed by c-Fos and its related proteins. Peak of the increased binding was 60 minutes in both hippocampus and cerebellum. Though expression of c-Fos and c-Jun were increased by ECS, there were no changes in AP-1 binding activities after ECS. AP-1 sites of IEGs were binded by CREB, regardless of ECS. CONCLUSION: There is a possibility that ECS induced IEG expression, and then incresed expression of NMDR1 by binding of expressed IEGs to the AP-1 site of NMDAR1. ECS did not increase AP-1 binding activities of IEGs. This suggests that the regulation of IEGs' expression can not be influenced mainly by AP-1 site.
