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In this study,cerebellar granule neurons were used to examine the role of nitric oxide on cell survival.The N-methyl-D-aspartic acid receptor antagonist,MK-801,and the soluble guanylate cyclase antagonist,1H-[1,2,4]oxadiazolo-[4,3-a] quinoxalin-1-one,decreased cell viability,induced caspase-3,and decreased phosphorylated-Akt levels,suggesting that blockade of nitric oxide production promotes apoptosis of differentiating cerebellar granule neurons.After administration of sodium nitroprusside,an endogenous nitric oxide donor,cell viability recovered,caspase-3 expression was decreased,and phosphorylated-Akt levels increased.This study provides direct evidence that nitric oxide can sustain the survival of developing cerebellar granule neurons in vitro through the nitric oxide-Akt pathway.Moreover,endogenous nitric oxide exerts these effects in a cyclic guanosine monophosphate-dependent manner while exogenous nitric oxide does so in a cyclic guanosine monophosphate-independent manner.
In this study, cerebellar granule neurons were used to examine the role of nitric oxide on cell survival. N-methyl-D-aspartic acid receptor antagonist, MK-801, and the soluble guanylate cyclase antagonist, 1H- [ 4] oxadiazolo- [4,3-a] quinoxalin-1-one, decreased cell viability, induced caspase-3, and decreased phosphorylated-Akt levels, suggesting that blockade of nitric oxide production promotes apoptosis of differentiating cerebellar granule neurons. After administration of sodium nitroprusside, an endogenous nitric oxide donor, cell viability recovered, caspase-3 expression was decreased, and phosphorylated-Akt levels increased. This study provides direct evidence that nitric oxide can sustain the survival of developing cerebellar granule neurons in vitro through the nitric oxide-Akt pathway. Moreover, endogenous nitric oxide exerts these effects in a cyclic guanosine monophosphate-dependent manner while exogenous nitric oxide does so in a cyclic guanosine monophosphate-independent manner.