<p>A characteristic nonlinear phenomenon wherein neuronal firing is enhanced following inhibition, post-inhibitory rebound (PIR), plays a crucial role in various neural functions, such as rhythm generation in central pattern generator (CPG) circuits that control locomotion. In this investigation on a unilateral CPG model for zebrafish locomotion, the interaction between PIR induced by disinhibition, and excitatory synaptic current results in reduced delay between firings of pacemaker neuron V2a and motoneuron (MN), i.e., faster propagation of excitation from V2a to MN. At first, to be consistent with experiment, firing for V2a and resting states for MN and inhibitory interneuron V1 are acquired by two-parameter bifurcation analysis. Then, since locating around the Hopf bifurcation, V2a and MN exhibit PIR facilitated by weakened calcium-dependent potassium current (<i>I</i>_KCa) during inhibition, presenting the potential dynamical influence of <i>I</i>_KCa on PIR. In the unilateral CPG with inhibition from the contralateral CPG ignored, increasing the strength and rise rate of excitatory synapse from V2a to MN significantly enhances synaptic current. This reduces the delay between V2a and MN firings, while V1 plays a minor role. Then, contralateral inhibitions, described by negative currents, are considered. Removal of a strong contralateral inhibition acting solely on V2a enhances PIR firing, strengthening excitatory synaptic current to MN and then shortening the delay. Additionally, contralateral inhibition to MN can further shorten the delay, as the disinhibition of MN occurs later than that of V2a, which are induced by the interaction between PIR and excitatory synaptic input. The dynamics and modulations for the faster propagation of excitation from pacemaker to motoneuron, containing the PIR and nonlinear interaction, are elucidated.</p>