Sherman A
Mathematical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.
Bull Math Biol. 1994 Sep;56(5):811-35. doi: 10.1007/BF02458269.
I seek to explain phenomena observed in simulations of populations of gap junction-coupled bursting cells by studying the dynamics of identical pairs. I use a simplified model for pancreatic beta-cells and decompose the system into fast (spike-generating) and slow subsystems to show how bifurcations of the fast subsystem affect bursting behavior. When coupling is weak, the spikes are not in phase but rather are anti-phase, asymmetric or quasi-periodic. These solutions all support bursting with smaller amplitude spikes than the in-phase case, leading to increased burst period. A key geometrical feature underlying this is that the in-phase periodic solution branch terminates in a homoclinic orbit. The same mechanism also provides a model for bursting as an emergent property of populations; cells which are not intrinsic bursters can burst when coupled. This phenomenon is enhanced when symmetry is broken by making the cells differ in a parameter.
我试图通过研究相同细胞对的动力学来解释在缝隙连接耦合的爆发性细胞群体模拟中观察到的现象。我使用了一个简化的胰腺β细胞模型,并将系统分解为快速(产生尖峰)和慢速子系统,以展示快速子系统的分岔如何影响爆发行为。当耦合较弱时,尖峰不同步,而是反相、不对称或准周期的。这些解都支持比同相情况具有更小幅度尖峰的爆发,从而导致爆发周期增加。其背后的一个关键几何特征是同相周期解分支终止于一个同宿轨道。同样的机制也为爆发作为群体的一种涌现特性提供了一个模型;非固有爆发性的细胞在耦合时可以爆发。当通过使细胞在一个参数上不同而打破对称性时,这种现象会增强。