NA+ CA2+ EXCHANGER MODULATES KAINATE-TRIGGERED CA2+ SIGNALING IN BERGMANN GLIAL-CELLS IN-SITU/

The role of sodium-calcium exchanger in calcium homeostasis in Bergman n glial cells in situ was investigated by monitoring cytoplasmic calci um ([Ca2+](i)) and sodium ([Na+](i)) concentrations. The [Ca2+](i) and [Na+](i) transients were measured either separately by using fluoresc ent indicators fura-2 and SBFI, respectively, or simultaneously using the indicators fluo-3 and SBFI. Since the removal of extracellular Na induced a relatively small (similar to 50 nM) elevation of [Ca2+](i), the Na+/Ca2+ exchanger seems to play a minor role in regulation of re sting [Ca2+](i). In contrast, kainate-triggered [Ca2+](i) increase was significantly suppressed by lowering of the extracellular Na+ concent ration ([Na+](o)). In addition, manipulations with [N-a+](o) dramatica lly affected the recovery of the kainate-induced [Ca2+](i) transients. Simultaneous recordings of [Ca2+](i) and [Na+](i) revealed that kaina te-evoked [Ca2+](i) transients were accompanied with an increase in [N a+](i). Moreover, kainate induced significantly larger [Ca2+](i) and s maller [Na+](i) transients under current-clamp conditions as compared to those recorded when the membrane voltage was clamped at -70 mV. The above results demonstrate that the Na+-Ca2+ exchanger is operative in Bergmann glial cells in situ and is able to modulate dynamically the amplitude and kinetics of [Ca2+](i) signals associated with an activat ion of ionotropic glutamate receptors.