Title : NMDA receptors and the differential ischemic vulnerability of hippocampal neurons.

Pub. Date : 2006 May

PMID : 16817862






4 Functional Relationships(s)
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1 Using an in vitro oxygen-glucose deprivation (OGD) model of ischemia, we found that N-methyl-D-aspartate (NMDA) responses were enhanced in the more susceptible CA1 pyramidal cells and transiently depressed in the resistant CA3 pyramidal cells. N-Methylaspartate carbonic anhydrase 1 Homo sapiens
2 Using an in vitro oxygen-glucose deprivation (OGD) model of ischemia, we found that N-methyl-D-aspartate (NMDA) responses were enhanced in the more susceptible CA1 pyramidal cells and transiently depressed in the resistant CA3 pyramidal cells. N-Methylaspartate carbonic anhydrase 1 Homo sapiens
3 The long-lasting potentiation of NMDA responses in CA1 cells was associated with delayed cell death and was prevented by blocking tyrosine kinase-dependent up-regulation of NMDA receptor function. N-Methylaspartate carbonic anhydrase 1 Homo sapiens
4 These results suggest that energy deprivation differentially shifts the intracellular equilibrium between the tyrosine kinase and phosphatase activities that modulate NMDA responses in CA1 and CA3 pyramidal cells. N-Methylaspartate carbonic anhydrase 1 Homo sapiens