The prefrontal cortex (PFC) exhibits prominent oscillatory activity already during early development. In the mouse PFC, these oscillations develop a beta band [15-30 Hz] component during the second postnatal week. These fast oscillations increase in frequency and amplitude with age until stabilizing in the adult-characteristic gamma band [30-80 Hz] during the fourth postnatal week. Abnormal development of fast prefrontal oscillations has been reported for mouse models of schizophrenia and autism. Here, we investigate potential drivers of PFC peak frequency acceleration through simulations of recurrent cortical networks with parameter values reflecting developmental changes. We first implement a “mature” reference recurrent cortical model using an integrate-and-fire network, with the LFP approximated from the synaptic currents. To simulate developmental changes, we alter network parameters individually with their values constrained by existing experimental measures across development. Slowing GABAA receptor kinetics to values observed in young mice decreases the peak frequency from 70 Hz at the mature state to 20 Hz, in agreement with the experimental data (Fig. 1A). Reducing the external input rate decreases the peak frequency too but also reduces the peak power (Fig. 1B). Modifying AMPA receptor kinetics (Fig. 1C) or the E:I balance causes only minor changes of the oscillation peak frequency. Contrary to experimental data, increasing the membrane capacitance or time constant (Fig. 1D) augments the peak frequency. These results indicate that the changes in peak oscillation frequency seen in the developing mouse PFC could be mainly mediated by faster GABAA receptor kinetics with age alongside higher external inputs.