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No attempts have yet been made to concurrently explore the contributions of extracellular and intracellular Ca<jats:sup>2+<\/jats:sup> to basal ganglionic transmission or LTP. Here, we investigate this subject using the superior cervical ganglion of the rat. To explore the extracellular Ca<jats:sup>2+<\/jats:sup> contribution, we evaluated basal transmission and LTP at different extracellular Ca<jats:sup>2+<\/jats:sup> concentrations. To assess intracellular Ca<jats:sup>2+<\/jats:sup> release, we explored the contribution of the calcium\u2010induced calcium release process by overactivation or blockade of ryanodine\u2010sensitive Ca<jats:sup>2+<\/jats:sup> receptor channel with caffeine, and also by blocking either IP3R with Xestospongin C or the sarco(endo)plasmic reticulum Ca<jats:sup>2+<\/jats:sup>\u2010ATPase pump with thapsigargin. Extracellular Ca<jats:sup>2+<\/jats:sup> affected ganglionic basal transmission and LTP to different extents. While 25% of the physiological Ca<jats:sup>2+<\/jats:sup> concentration supported 80% of basal transmission, 50% of normal Ca<jats:sup>2+<\/jats:sup> was required to achieve 80% of LTP. Notably, disruption of intracellular Ca<jats:sup>2+<\/jats:sup> release by all the drugs tested apparently did not affect basal ganglionic transmission but impaired LTP. We conclude that basal transmission requires only a small level of Ca<jats:sup>2+<\/jats:sup> entry, while LTP expression not only requires more Ca<jats:sup>2+<\/jats:sup> entry but is also dependent on Ca<jats:sup>2+<\/jats:sup> release from intracellular stores. \u00a9 2007 Wiley Periodicals, Inc. 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