Cooperative maintenance of cellular identity in systems with intercellular communication defects

The cooperative dynamics of cellular populations emerging from the underlying interactions determines cellular functions and thereby their identity in tissues. Global deviations from this dynamics, on the other hand, reflect pathological conditions. However, how these conditions are stabilized from dysregulation on the level of the single entities is still unclear. Here, we tackle this question using the generic Hodgkin-Huxley type of models that describe physiological bursting dynamics of pancreatic β-cells and introduce channel dysfunction to mimic pathological silent dynamics. The probability for pathological behavior in β-cell populations is ∼100% when all cells have these defects, despite the negligible size of the silent state basin of attraction for single cells. In stark contrast, in a more realistic scenario for a mixed population, stabilization of the pathological state depends on the size of the subpopulation which acquired the defects. However, the probability to exhibit stable pathological dynamics in this case is less than 10%. These results, therefore, suggest that the physiological bursting dynamics of a population of β-cells is cooperatively maintained, even under intercellular communication defects induced by dysfunctional channels of single cells.