THE STIMULUS-EVOKED RELEASE OF GLUTAMATE AND GABA FROM BRAIN SUBREGIONS FOLLOWING TRANSIENT FOREBRAIN ISCHEMIA IN THE RAT

The release of glutamate and GABA in response to K+ depolarization was determined for tissue prisms prepared from brain subregions removed f rom rats following 30 min of forebrain ischemia or recirculation perio ds up to 24 h. There were statistically significant effects of this tr eatment on release of both amino acids from samples of the dorsolatera l striatum, an area developing selective neuronal degeneration. Howeve r, for at least the first 3 h of recirculation the calcium-dependent a nd calcium-independent release of both amino acids in this region were similar to pre-ischemic values. Differences were observed under some conditions at longer recirculation times. In particular there was a de crease in calcium-dependent GABA release at 24 h of recirculation and a trend towards increased release of glutamate at 6 h of recirculation and beyond. No statistically significant differences were seen in sam ples from the paramedian neocortex, a region resistant to post-ischemi c damage. These results suggest that changes in the ability to release glutamate and GABA in response to stimulation are not necessary for t he development of neurodegeneration in the striatum but rather that re lease of these amino acids may be modified as a result of the degenera tive process.