[Signaling pathway of BDNF protecting embryonic cortical neurons from hypoxia].
OBJECTIVE
To investigate the changes of TrkB and Ras-MAPK in brain-derived neurotrophic factor (BDNF) protecting the embryonic rat cerebral cortical neurons against hypoxia-induced neurotoxicity.


METHODS
The immunofluorescence technique, laser scanning confocal microscope and half-quantitative analysis were done to explore the changes of the intracellular levels of tyrosine kinase B (TrkB), phosphorylated TrkB and the mitogen-activated protein kinase (MAPK) in rat embryonic cortical neurons cultured in different time groups of hypoxia with or without BDNF pretreatment.


RESULTS
The fluorescent intensity of TrkB and phosphorylated TrkB in the cytoplasm and the fluorescent intensity of MAPK in both cytoplasm and cell nucleus of the neurons were significantly increased in the presence of BDNF (P < 0.05), the fluorescent intensity of neurons pretreated with BDNF 24 h before the hypoxia culture was stronger than those with BDNF just before the hypoxia culture (P < 0.05).


CONCLUSIONS
The Ras-MAPK approach may be the major signal transferring way of BDNF in protecting the cortical neurons from hypoxia-induced neurotoxicity. The approach of signal transferring begins with tyrosine phosphorylation of TrkB receptors.
Wang
Zhi-ling
ZL
Department of Pediatrics, West China Second Hospital, Sichuan University, Chengdu, China.
Mao
Meng
M
Zhou
Hui
H
Li
Sheng-fu
SF
Yu
Dan
D
D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism*; D015687:Cell Hypoxia; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000166:cytology*; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010766:Phosphorylation; D051381:Rats; D020813:Receptor, trkB / Q000378:metabolism; D015398:Signal Transduction; D018631:ras Proteins / Q000378:metabolism
D019208:Brain-Derived Neurotrophic Factor; D020813:Receptor, trkB; D020928:Mitogen-Activated Protein Kinases; D018631:ras Proteins