Abstract
The paradoxical phenomena that excitatory modulation does not enhance but reduces or inhibitory modulation not suppresses but promotes neural firing activities have attracted increasing attention. In the present study, paradoxical phenomena induced by both fast excitatory and inhibitory autapses in a "Fold/Big Homoclinic" bursting are simulated, and the corresponding nonlinear and biophysical mechanisms are presented. Firstly, the enhanced conductance of excitatory autapse induces the number of spikes per burst and firing rate reduced, while the enhanced inhibitory autapse cause both indicators increased. Secondly, with fast-slow variable dissection, the burst of bursting is identified to locate between a fold bifurcation and a big saddle-homoclinic orbit bifurcation of the fast subsystem. Enhanced excitatory or inhibitory autapses cannot induce changes of both bifurcation points, i.e., burst width. However, width of slow variable between two successive spikes within a burst becomes wider for the excitatory autapse and narrower for the inhibitory autapse, resulting in the less and more spikes per burst, respectively. Last, the autaptic current of fast autapse mainly plays a role during the peak of action potential, differing from the slow autaptic current with exponential decay, which can play roles following the peak of action potential. The fast excitatory autaptic current enhances the amplitude of the action potential and reduces the repolarization of the action potential to lengthen the interspike interval (ISI) of the spiking of the fast subsystem, resulting in the wide width of slow variable between successive spikes. The fast inhibitory autaptic current reduces the amplitude of action potential and ISI of spiking, resulting in narrow width of slow variable. The novel example of the paradoxical responses for both fast modulations and nonlinear mechanism extend the contents of neurodynamics, which presents potential functions of the fast autapse.