[Study on the mechanism of glutamate mediated neurotoxicity by cortical neuron culture technique in vitro].
This study was intended to further explain the mechanism of glutamate (Glu) mediated neurotoxicity. The concentrations of TCa and Ca2+ i were measured in 32 cortical neuron cultures, which were divided into four groups: normal control group (n = 8); 0.5 mmol/L Glu group (Glu group n = 8); 0.5 mmol/L Glu + 100 mmol/L Nimodipine group (antagonist I, n = 8); 0.5 mmol/L Glu + 12 mumol/L MK-801 group (antagonist II, n = 8). The results showed that TCa and Ca2+ i concentrations in Glu group were significantly higher than those in normal control group (P < 0.05); TCa and Ca2+i in both antagonist I and II groups were evidently lower than those in Glu group (P < 0.05); No difference was found between antagonist I and II groups. The results suggest that Glu neurotoxicity is due to the intracellular calcium overload, which may be from the pathway of voltage-dependent calcium channels (VDCCs) and NMDA receptor-operated channels (NROCs).
Zeng
Z
Z
Department of Pediatrics, Second Affiliated Hospital, WCUMS, Chengdu 610041.
Li
W
W
Yao
Y
Y
Chen
N
N
D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000187:drug effects; D002478:Cells, Cultured; D002540:Cerebral Cortex / Q000378:metabolism / Q000473:pathology*; D004622:Embryo, Mammalian; D005260:Female; D018698:Glutamic Acid / Q000633:toxicity*; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D011247:Pregnancy; D011897:Random Allocation; D051381:Rats
D015220:Calcium Channels; D018698:Glutamic Acid; D002118:Calcium