Ca²⁺ is vital for release of neurotransmitters and trophic factors from peripheral sensory nerve terminals (PSNTs), yet Ca²⁺ regulation in PSNTs remains unexplored. To elucidate the Ca²⁺ regulatory mechanisms in PSNTs, we determined the effects of a panel of pharmacological agents on electrically-evoked Ca²⁺ transients in rat corneal nerve terminals (CNTs) in vitro that had been loaded with the fluorescent Ca²⁺ indicator, Oregon Green 488 BAPTA-1 dextran or fura-2 dextran in vivo. Inhibition of SR/ER Ca²⁺CATPase (SERCA), disruption of mitochondrial Ca²⁺ uptake, or inhibition of the sodium/calcium exchanger (NCX) did not measurably alter the amplitude or decay kinetics of the electrically-evoked Ca²⁺ transients in CNTs. By contrast, inhibition of the plasma membrane Ca²⁺CATPase (PMCA) by increasing the pH slowed the decay of the Ca²⁺ transient by 2-fold. Surprisingly, the energy for ion transport across the plasma membrane of CNTs is predominantly from glycolysis rather than mitochondrial respiration, as evidenced by the observation that Ca²⁺ transients were suppressed by iodoacetate but unaffected by mitochondrial inhibitors. These observations indicate that, following electrical activity, the PMCA is the predominant mechanism of Ca²⁺ clearance from the cytosol of CNTs and glycolysis is the predominant source of energy.