Previous study demonstrated that, in hippocampal neuron/glia mixed cultures,
glucocorticoids (GCs) enhanced extracellular overflow of [3H]
D-aspartate [3H]D-Asp) by decreasing its uptake, thereby aggravating cell death during
cyanide-induced
ischemia. Since neuronal and glial cells respond to ischemic insult and GC differently, this study further evaluated the relative significance of these cells in GC endangering ischemic cell death. Using D-[2,3-3H]
aspartic acid ([3H]D-Asp) as a tracer, it was found that
corticosterone (CORT, the physiological GC in rat) enhanced the overflow of extracellular [3H]D-Asp in astrocyte cultures and, to a lesser extent, in neuron-enriched cultures during
cyanide-induced
ischemia. Analysis of [3H]D-Asp uptake kinetics indicates that CORT reduced the maximum uptake rate in cultured astrocyte, but not in neurons, after
cyanide exposure. It is concluded that, during
cyanide-induced
ischemia, CORT might mainly the ability of astrocytes to clear
excitatory amino acids from the synapse, thus exacerbating the damaging cascade of these
amino acids.