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We have used rapid confocal microscopy to investigate the mechanism of Ca2+ signals in individual dendritic spines of hippocampal CA1 pyramidal cells. The experiments focused on the signals that occur during single weak synaptic responses that were subthreshold for triggering postsynaptic action potentials. These Ca2+ signals were not strongly affected by blocking the EPSPs with the AMPA receptor antagonist CNQX. The signals were also not strongly reduced by blocking T-type voltage-gated Ca2+ channels (VGCCs) with Ni2+or by blocking a broad range of VGCCs with intracellular D890. The spine Ca2+ signals were blocked by NMDA receptor channel (NMDAR) antagonist and had the voltage dependence characteristic of these channels. Neither ryanodine nor cyclopiazonic acid (CPA), substances known to deplete intracellular Ca2+ stores, substantially reduced the amplitude of synaptically evoked Ca2+ signals. CPA slowed the recovery phase of Ca2+ signals in spines produced by synaptic stimulation or by backpropagating action potentials, suggesting a role of intracellular stores in Ca2+reuptake. Thus, we find that Ca2+ release from intracellular stores is not required to produce spine Ca2+ signals. We conclude that synaptic Ca2+ signals in spines are primarily caused by Ca2+ entry through NMDARs. Although these channels are largely blocked by Mg2+ at voltages near the resting potential, they can nevertheless produce significant Ca2+ elevation. The resulting Ca2+ signals are an integral component of individual evoked or spontaneous synaptic events and may be important in the maintenance of synaptic function.

NMDA Receptor-Mediated Subthreshold Ca2+Signals in Spines of Hippocampal Neurons

NMDA Receptor-Mediated Subthreshold Ca²⁺Signals in Spines of Hippocampal Neurons