Fast-spiking parvalbumin-expressing basket cells (BCs) represent a major type of inhibitory interneuron in the hippocampus. These cells inhibit principal cells in a temporally precise manner and are involved in the generation of network oscillations. Although BCs show a unique expression profile of Ca2+ permeable receptors, Ca2+ binding proteins, and Ca2+-dependent signaling molecules, physiological Ca2+ signaling in these interneurons has not been investigated. To study action potential (AP)-induced dendritic Ca2+ influx and buffering, we combined whole-cell patch-clamp recordings with ratiometric Ca2+ imaging from the proximal apical dendrites of rigorously identified BCs in acute slices, using the high-affinity Ca2+ indicator fura-2 or the low-affinity dye fura-FF. Single APs evoked dendritic Ca2+ transients with small amplitude. Bursts of APs evoked Ca2+ transients with amplitudes that increased linearly with AP number. Analysis of Ca2+ transients under steady-state conditions with different fura-2 concentrations and during loading with 200 µM fura-2 indicated that the endogenous Ca2+-binding ratio was ~ 200 (kappaS = 202 ± 26 for the loading experiments). The peak amplitude of the Ca2+ transients measured directly with 100 µM fura-FF was 39 nM AP-1. At ~23°C, the decay time constant of the Ca2+ transients was 390 ms, corresponding to an extrusion rate of ~600 s-1. At 34°C, the decay time constant was 203 ms and the corresponding extrusion rate was ~1100 s-1. At both temperatures, continuous theta-burst activity with 3 – 5 APs per theta cycle, as occurs in vivo during exploration, led to a moderate increase in the global Ca2+ concentration that was proportional to AP number, whereas more intense stimulation was required to reach micromolar Ca2+ concentrations and to shift Ca2+ signaling into a nonlinear regime. In conclusion, dentate gyrus BCs show a high endogenous Ca2+-binding ratio, a small AP-induced dendritic Ca2+ influx, and a relatively slow Ca2+ extrusion. These specific buffering properties of BCs will sharpen the time course of local Ca2+ signals, while prolonging the decay of global Ca2+ signals.