Activity-Evoked Capacitative Ca2+Entry: Implications in Synaptic Plasticity

Abstract

The Ca 2+influx controlled by intracellular Ca 2+stores, called store-operated Ca 2+entry (SOC), occurs in various eukaryotic cells, but whether CNS neurons are endowed with SOC capability and how they may operate have been contentious issues. Using Ca 2+imaging, we present evidence for the presence of SOC in cultured hippocampal pyramidal neurons. Depletion of internal Ca 2+stores by thapsigargin caused intracellular Ca 2+elevation, which was prevented by SOC channel inhibitors 2-aminoethoxydiphenyl borate (2-APB),SKF96365, and La 3+. Interestingly, these inhibitors also accelerated the decay of NMDA-induced Ca 2+transients without affecting their peak amplitude. In addition, SOC channel inhibitors attenuated tetanus-induced dendritic Ca 2+accumulation and long-term potentiation at Schaffer collateral-CA1 synapses in hippocampal slice preparations. These data suggest a novel link between ionotropic receptor-activated SOC and neuroplasticity.