Intracellular calcium (Cai) regulates a broad spectrum of determinant neuronal processes and therefore must be tighly regulated. Calcium binding proteins (CBP) play a key role in this regulation. Among these, parvalbumin (PV) is particularly enriched in striatal fast spiking interneurons (FSI). FSI exert a powerful feedforward inhibition on striatal projection neurons, orchestrating their fine spike timing. We investigated the role of parvalbumin on the electroresponsiveness of these interneurons by using the amphotericin-perforated patch configuration of the patch-clamp technique. We performed current clamp recordings of single FSI from coronal striatal slices of wild type mice (WT) and PV-knock-out mice (PVKO) aged between 18–25 days-old. Voltage responses obtained by increasing injected current intensities generated slopes of the linear part of current-frequency plots. These slopes reflect the intrinsic FSI excitability. A significant increase (p<0.05) has been found in excitability slopes for PVKO mice (0.81±0.1 Hz.pA-1, n=6) vs. WT mice (0.51±0.05 Hz.pA-1, n=6). Furthermore, maximal spiking frequencies are higher in PVKO mice (135.71±9.38 Hz) compared to WT mice (102.66±12.44 Hz , p<0.05). Finally, we propose a mathematical model providing a link between our experimental observations about the electrical activity of FSI and a decrease in cytosolic Cai buffering capacity induced by the PV deletion.