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- W2972095671 abstract "In the present study, we investigated the mechanisms underlying the mediation of iron transport by L-type Ca2+ channels (LTCCs) in primary cultured ventral mesencephalon (VM) neurons from rats. We found that co-treatment with 100 µmol/L FeSO4 and MPP+ (1-methyl-4-phenylpyridinium) significantly increased the production of intracellular reactive oxygen species, decreased the mitochondrial transmembrane potential and increased the caspase-3 activation compared to MPP+ treatment alone. Co-treatment with 500 µmol/L CaCl2 further aggravated the FeSO4-induced neurotoxicity in MPP+-treated VM neurons. Co-treatment with 10 µmol/L isradipine, an LTCC blocker, alleviated the neurotoxicity induced by co-application of FeSO4 and FeSO4/CaCl2. Further studies indicated that MPP+ treatment accelerated the iron influx into VM neurons. In addition, FeSO4 treatment significantly increased the intracellular Ca2+ concentration. These effects were blocked by isradipine. These results suggest that elevated extracellular Ca2+ aggravates iron-induced neurotoxicity. LTCCs mediate iron transport in dopaminergic neurons and this, in turn, results in elevated intracellular Ca2+ and further aggravates iron-induced neurotoxicity." @default.
- W2972095671 created "2019-09-12" @default.
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- W2972095671 date "2019-09-03" @default.
- W2972095671 modified "2023-10-01" @default.
- W2972095671 title "L-type Calcium Channels are Involved in Iron-induced Neurotoxicity in Primary Cultured Ventral Mesencephalon Neurons of Rats" @default.
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- W2972095671 doi "https://doi.org/10.1007/s12264-019-00424-2" @default.
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