【摘 要】
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In the present study,we investigated the mechanisms underlying the mediation of iron transport by Ltype Ca2+ channels (LTCCs) in primary cultured ventral mesencephalon (VM) neurons from rats.We found that cotreatment with 100 μtmol/L FeSO4 and MPP+ (1-met
【机 构】
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Department of Physiology, School of Basic Medicine, Qingdao University, Qingdao 266071, China;Instit
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In the present study,we investigated the mechanisms underlying the mediation of iron transport by Ltype Ca2+ channels (LTCCs) in primary cultured ventral mesencephalon (VM) neurons from rats.We found that cotreatment with 100 μtmol/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 pmol/L CaCl2 further aggravated the FeSO4-induced neurotoxicity in MPP+-treated VM neurons.Co-treatment with 10 μtmol/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 ironinduced neurotoxicity.LTCCs mediate iron transport in dopaminergic neurons and this,in turn,results in elevated intracellular Ca2+ and further aggravates iron-induced neurotoxicity.
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