The neocortex is built up from homologous neuron types, but neurons exhibit between-species differences in gene expression, molecular profile, and electrical function. Purpose of these specializations is not well understood. In human neocortex, fast-spiking interneurons have high electrical excitability compared to their rodent counterparts. This slows down time course for cell membrane potential changes, and in theory, makes human fast-spiking neurons slower than rodent cells to process electrical input signals and generate action potential (AP). However, human neurons are nearly as fast with the “in-out” -function as their rodent counterparts indicating that some mechansisms have evolved in human cells to facilitate electrical input-output transformation. Herein, microelectrode recordings in neocortical tissue resected in brain surgery show that human fast-spiking parvalbumin (pv) neurons exhibit lowered threshold for APs, and this correlates with slow electrical time course in cell soma. Confocal microscope immunofluorescence study reveals low level of inhibitory Kv1.1 potassium channel in AIS in human pv cells. In addition, most pv cells in human lack mRNA for (KCN1A) gene encoding the ion channel. These both are strong in mouse pv cells. Human pv cells also have long axon initial segment (AIS), a specialized structure triggering action potential. pv cell computational cable model demonstrates that AP firing threshold is effectively lowered by reduced Kv1 channels in the AIS and by increasing the AIS length, offering an explanation to the firing threshold species difference. Lowered AP firing level also shortens AP generation delay in the human pv cell computational model.