P30: Effects of Hemin on Ca2+Influx in Neurons of C57BL/6 Mouse Brain

Excitotoxicity results in a significant increase in Ca2+ influx; essentially from open N-Methyl-D-aspartate receptors (NMDARs) channels that cause a secondary rise in the intracellular Ca2+ concentration. It is correlated with neuronal death induced by Ca2+ overload. Dysfunction of NMDARs is associated with excitotoxic neuronal death in neurodegenerative disorders. In this study, the effects of hemin on Ca2+ permeability in neurons of C57BL/6 mouse brain examined. Isolated from 1-dayold C57BL/6 mice, were cultured in serum-free media. Cells were maintained in growth medium at 37◦C in 95% air/5% CO2 for 2 weeks in vitro before treatment. Primary neurons were cultured in serum-free media were treated with hemin (0, 12.5, 25, 50, 75,100 &mu;M) for 18 (h). Intensity of calcium fluorescence was reduced in treated cultures with hemin (100, 86, 78.5, 60, 56, 46%, respective to the concentrations stated previously; P<0.05 for all). Hemin increased Ca2+ influx in cultured neurons. NMDAR stimulation by hemin increased the activating of NMDARs and Ca2+ influx in the cultured neurons. Therefore, heminis cytotoxic due to increase of intracellular Ca2+ influx. &nbsp;