Effect of zinc on the corticosterone-induced injury of primary cultured rat hippocampal neurons.
- Author:
Zhan-Hui GENG
1
;
Yi-Yong CHENG
;
Xiu-Ling MA
;
Shu-Tian LI
Author Information
1. Institute of Health and Environmental Medicine, Academy of Military Medical Sciences, Tianjin 300050.zhanghuigeng@yahoo.com.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Apoptosis;
drug effects;
Cells, Cultured;
Corticosterone;
pharmacology;
Hippocampus;
pathology;
Neurons;
pathology;
Neuroprotective Agents;
pharmacology;
RNA, Messenger;
biosynthesis;
genetics;
Rats;
Receptors, N-Methyl-D-Aspartate;
biosynthesis;
classification;
genetics;
Reverse Transcriptase Polymerase Chain Reaction;
Zinc;
pharmacology
- From:
Acta Physiologica Sinica
2003;55(6):736-741
- CountryChina
- Language:Chinese
-
Abstract:
The effect of zinc on the damage of primary cultured hippocampal neurons induced by corticosterone (CORT) was studied. Neuronal injury and expression of NMDA receptor subunits (NR1,NR2A,NR2B) mRNA were detected by using in situ staining and RT-PCR, respectively. Neurons treated with 5 micromol/L CORT for 24 h showed decreased survival rates and increased apoptotic rates compared with the controls; co-application of CORT and 10 or 100 micromol/L Zn(2+) attenuated apoptotic rates while 250 micromol/L Zn(2+) worsened CORT-induced neuronal injury. Expression of NR1, NR2B mRNA in neurons treated by 5 micromol/L CORT for 24 h was significantly increased, while those concurrently added with 10 or 100 micromol/L Zn(2+) showed no changes. No statistic difference in NR2A mRNA was obtained under any treatment. These results suggest that zinc can bilaterally regulate neuronal injuries induced by CORT, among while NMDA receptors probably play an important role.
