N-methyl-D-aspartate and hypoxia induced Ca2+-changes in the CA1 region of the hippocampal slice.
Hypoxic neuronal depolarization was accompanied by a large decrease in extracellular [Ca2+]. After reoxygenation, the time at which [Ca2+] normalized was correlated with the extent of recovery of N-methyl-D-aspartate (NMDA) and synaptic responses. There was no evidence that the NMDA receptor system was more disrupted following hypoxia than the receptors involved in synaptic transmission. The Na+/K+ pump appeared to be better able to recover from hypoxia than the NMDA responses or synaptic transmission.
D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D006168:Guinea Pigs; D006624:Hippocampus / Q000187:drug effects / Q000503:physiopathology*; D002534:Hypoxia, Brain / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials; D016202:N-Methylaspartate
D001224:Aspartic Acid; D016202:N-Methylaspartate; D002118:Calcium