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
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.
