Qi Changsheng, Li Yuye, Gu Huaguang, Yang Yongxia
College of Chemistry and Life Sciences, Chifeng University, Chifeng, 024000 China.
College of Mathematics and Computer Science, Chifeng University, Chifeng, 024000 China.
Cogn Neurodyn. 2023 Aug;17(4):1093-1113. doi: 10.1007/s11571-022-09872-5. Epub 2022 Aug 21.
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.
兴奋性调制并未增强反而降低、抑制性调制并未抑制反而促进神经放电活动的这种矛盾现象已引起越来越多的关注。在本研究中，模拟了“折叠/大同宿”爆发中快速兴奋性和抑制性自突触诱导的矛盾现象，并给出了相应的非线性和生物物理机制。首先，兴奋性自突触电导增强导致每个爆发的尖峰数量和放电率降低，而抑制性自突触电导增强则使这两个指标增加。其次，通过快慢变量分解，确定爆发的爆发位于快速子系统的折叠分岔和大鞍点同宿轨道分岔之间。增强的兴奋性或抑制性自突触不会引起两个分岔点（即爆发宽度）的变化。然而，爆发内两个连续尖峰之间的慢变量宽度对于兴奋性自突触变宽，对于抑制性自突触变窄，分别导致每个爆发的尖峰更少和更多。最后，快速自突触的自突触电流主要在动作电位峰值期间起作用，这与具有指数衰减的慢自突触电流不同，慢自突触电流可在动作电位峰值之后起作用。快速兴奋性自突触电流增强动作电位的幅度并减少动作电位的复极化，以延长快速子系统放电的峰峰间隔（ISI），导致连续尖峰之间的慢变量宽度变宽。快速抑制性自突触电流降低动作电位的幅度和放电的ISI，导致慢变量宽度变窄。快速调制和非线性机制的矛盾反应的新例子扩展了神经动力学的内容，展示了快速自突触的潜在功能。
