Intracellular Ca2+ overload and the following Ca2+-toxicity are an important mechanism underlying ischemic brain injury.However,recent clinical trials using antagonists of the N-methyl-daspartate(NMDA) to prevent isch...Intracellular Ca2+ overload and the following Ca2+-toxicity are an important mechanism underlying ischemic brain injury.However,recent clinical trials using antagonists of the N-methyl-daspartate(NMDA) to prevent ischemic brain injury in humans have been largely disappointing.Activation of glutamate receptors resulting in intracellular Ca2+ overload and excitotoxicity couldn’t explain the whole process of ischemic brain injury,and emerging new studies have suggested that activation of several glutamate receptor-independent Ca2+-toxicity pathways also contribute to ischemic brain injury.This review focus on the roles of acid sensing ion channels(ASICs),Na+-Ca2+ exchanger(NCX) and transient receptor potential(TRP) channels in the ischemic brain injury.展开更多
We determined whether La3+ enter human peripheral blood lymphocytes via Na+/Ca2+ exchanger (measured with fura-2). We first compared the sensitivity of fura-2 with La3+ and Ca2+, the result indicates that the sensitiv...We determined whether La3+ enter human peripheral blood lymphocytes via Na+/Ca2+ exchanger (measured with fura-2). We first compared the sensitivity of fura-2 with La3+ and Ca2+, the result indicates that the sensitivity of fura-2 for La3+ is much greater than for Ca2+. La3+ forms a 1:1 La3+-fura-2 complex (apparent dissociation constant = 1.7x10(-12) mol/L, pH 7.05). Ouabain-pretreated cells, suspended in Na+-free medium, showed that La3+ can enter human lymphocytes via the Na-i(+)/Ca2+ (La3+)(o) exchanger and is found to be about 10(-12) mol/L in cells exposed to 0.4 mmol/L La3+. Otherwise, the higher concentration (0.1 mmol/L) blocks the Na-i(+)/Ca2+(La3+)(o) exchange-mediated influx of Ca2+, but the lower concentration (0.01 mmol/L) appears to increase Ca2+ entry.展开更多
文摘Intracellular Ca2+ overload and the following Ca2+-toxicity are an important mechanism underlying ischemic brain injury.However,recent clinical trials using antagonists of the N-methyl-daspartate(NMDA) to prevent ischemic brain injury in humans have been largely disappointing.Activation of glutamate receptors resulting in intracellular Ca2+ overload and excitotoxicity couldn’t explain the whole process of ischemic brain injury,and emerging new studies have suggested that activation of several glutamate receptor-independent Ca2+-toxicity pathways also contribute to ischemic brain injury.This review focus on the roles of acid sensing ion channels(ASICs),Na+-Ca2+ exchanger(NCX) and transient receptor potential(TRP) channels in the ischemic brain injury.
基金The authors acknowledge the support of the National Natural Scicnce Foundation of ChinaProvincial Natural Science Foundation of Shanxi.
文摘We determined whether La3+ enter human peripheral blood lymphocytes via Na+/Ca2+ exchanger (measured with fura-2). We first compared the sensitivity of fura-2 with La3+ and Ca2+, the result indicates that the sensitivity of fura-2 for La3+ is much greater than for Ca2+. La3+ forms a 1:1 La3+-fura-2 complex (apparent dissociation constant = 1.7x10(-12) mol/L, pH 7.05). Ouabain-pretreated cells, suspended in Na+-free medium, showed that La3+ can enter human lymphocytes via the Na-i(+)/Ca2+ (La3+)(o) exchanger and is found to be about 10(-12) mol/L in cells exposed to 0.4 mmol/L La3+. Otherwise, the higher concentration (0.1 mmol/L) blocks the Na-i(+)/Ca2+(La3+)(o) exchange-mediated influx of Ca2+, but the lower concentration (0.01 mmol/L) appears to increase Ca2+ entry.
