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The Journal of Neuroscience, August 27, 2003, 23(21):7737-7741

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

Atsushi Baba, Takuya Yasui, Shigeyoshi Fujisawa, Ryuji X. Yamada, Maki K. Yamada, Nobuyoshi Nishiyama, Norio Matsuki, and Yuji Ikegaya

Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Tokyo 113-0033, Japan

The Ca²⁺ influx controlled by intracellular Ca²⁺ stores, called store-operated Ca²⁺ 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 Ca²⁺ imaging, we present evidence for the presence of SOC in cultured hippocampal pyramidal neurons. Depletion of internal Ca²⁺ stores by thapsigargin caused intracellular Ca²⁺ elevation, which was prevented by SOC channel inhibitors 2-aminoethoxydiphenyl borate (2-APB), SKF96365, and La³⁺. Interestingly, these inhibitors also accelerated the decay of NMDA-induced Ca²⁺ transients without affecting their peak amplitude. In addition, SOC channel inhibitors attenuated tetanus-induced dendritic Ca²⁺ 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.

Key words: store-operated calcium entry; NMDA; glutamate receptor; long-term potentiation; hippocampus; transient receptor potential channel

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Received May 28, 2003; revised June 25, 2003; accepted July 8, 2003.

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