The Ca 2ϩ influx controlled by intracellular Ca 2ϩ stores, called store-operated Ca 2ϩ 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 2ϩ imaging, we present evidence for the presence of SOC in cultured hippocampal pyramidal neurons. Depletion of internal Ca 2ϩ stores by thapsigargin caused intracellular Ca 2ϩ elevation, which was prevented by SOC channel inhibitors

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... oxydiphenyl borate (2-APB), SKF96365, and La 3ϩ . Interestingly, these inhibitors also accelerated the decay of NMDA-induced Ca 2ϩ transients without affecting their peak amplitude. In addition, SOC channel inhibitors attenuated tetanus-induced dendritic Ca 2ϩ 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.