Multiple calcium signaling pathways, including intracellular calcium release that is mediated by inositol triphosphate (IP3) or ryanodine calcium store receptors, seem to be involved in CA1 hippocampal synaptic plasticity. We have addressed the role of dendritic calcium release in short- and long-term potentiation (STP and LTP) using thapsigargin, which depletes intracellular calcium stores. Measuring Fura-2 calcium signals and extracellular field potentials, we have found that thapsigargin did not affect single pre-tetanus calcium transients but reduced tetanically evoked calcium changes. The latter effect prevented the formation of short- and long-lasting calcium enhancements. These results are consistent with the idea that intracellular calcium release is not involved in baseline synaptic transmission but is essential for those forms of synaptic plasticity.