CoCl2-induced enhancement of glucose transport activity in mediating hypoxic tolerance in cultured hippocampal neurons.
- Author:
Shun YU
1
;
Ming FAN
;
Tong ZHAO
;
Ai-Shi DING
;
Fu-Zhuang WANG
Author Information
1. Beijing Institute of Geriatrics, Xuanwu Hospital of Capital University of Medical Sciences, Beijing 100053.
- Publication Type:Journal Article
- MeSH:
Animals;
Animals, Newborn;
Cell Hypoxia;
Cell Survival;
drug effects;
Cells, Cultured;
Cobalt;
pharmacology;
Glucose Transporter Type 1;
metabolism;
Glucose Transporter Type 3;
metabolism;
Hippocampus;
cytology;
Hypoxia;
metabolism;
Neurons;
drug effects;
metabolism;
Organometallic Compounds;
pharmacology;
RNA, Messenger;
genetics;
Rats;
Rats, Wistar
- From:
Acta Physiologica Sinica
2002;54(6):508-512
- CountryChina
- Language:Chinese
-
Abstract:
The effect of CoCl(2) pretreatment on glucose transport activity of cultured newborn rat hippocampal neurons and its role in neuronal hypoxic tolerance were observed. The results showed that the 2-deoxy-D-[1-(3)H ]glucose uptake rate and the mRNA expressions of glucose transporters (GLUT1 and GLUT3) in the hippocampal neurons were significantly increased after a 24-hour pretreatment with CoCl(2). The cell injury induced by 6-hour or 8-hour hypoxic exposure was also greatly reduced by CoCl(2) pretreatment. The protective effect of CoCl(2) on the neurons was largely abolished by cytochalasin B, a specific inhibitor of glucose transporters. The results suggest that CoCl(2) can increase mRNA expressions of GLUT1 and GLUT3 and glucose transporter activity of the neurons, which may be an important mechanism for the increased tolerance of the neurons to hypoxia.
