Brief Communication Activity-Evoked Capacitative Ca Entry: Implications in Synaptic Plasticity

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 receptoractivated SOC and neuroplasticity.