The cooperative dynamics of cellular populations emerging from the underlying interactions determines cellular functions, and thereby their identity in tissues. Global deviations of this dynamics on the other hand reflects pathological conditions. However, how these conditions are stabilized from dis-regulation on the level of the single entities is still unclear. Using generic Hodgkin-Huxley type of models , we investigate here how channel defects in single beta-cells affect the intercellular communication, and whether the collective dynamicsof the population can be thereby influenced. We identify a stark contrast between the dynamical behavior of homogeneous and heterogenous populations of cells. Whereas in the first case, when all of the cells acquired channel defects, a coupling interval can be found for which the pathological dynamics is stabilized and will be exhibited with \approx 100\sim100 \\%DIF < probability, in a heterogenous population, at least N/2+1 cells must have the channel defects in order for the pathological dynamics to be stabilizied. The numerical simulations demonstrated however that the probability to exhibit the pathological dynamics in this case is maintained at <10\\%, even when the population contains only a single cell that displays physiological dynamics. This results therefore suggest that the physiological bursting dynamics of a population of beta-cells is cooperatively regulated, even when single-cells acquire disfunctional channels that induce intercellular communication defects.abstract %DIF > when all cell 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 heterogeneous population, stabilization of the pathological state depends on the size of the sub-population which acquired the defects. However, the probability to exhibit stable pathological dynamics in this case is less than \sim10\\%. These results therefore suggest that the physiological bursting dynamics of a population of beta-cells is cooperatively regulated, even under intercellular communication defects induced by dis-functional channels of single-cells.
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 reflects pathological conditions. However, how these conditions are stabilized from dis-regulation on the level of the single entities is still unclear. Here we tackle this question using generic Hodgkin-Huxley type of models that describe physiological bursting dynamics of pancreatic beta-cells , and introduce channel dis-function to mimic pathological silent dynamics. The probability for pathological behavior in beta-cell populations is\sim100 \\%DIF < probability, in a heterogenous population, at least N/2+1 cells must have the channel defects in order for the pathological dynamics to be stabilizied. The numerical simulations demonstrated however that the probability to exhibit the pathological dynamics in this case is maintained at <10\\%, even when the population contains only a single cell that displays physiological dynamics. This results therefore suggest that the physiological bursting dynamics of a population of beta-cells is cooperatively regulated, even when single-cells acquire disfunctional channels that induce intercellular communication defects.abstract %DIF > when all cell 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 heterogeneous population, stabilization of the pathological state depends on the size of the sub-population which acquired the defects. However, the probability to exhibit stable pathological dynamics in this case is less than \sim10\\%. These results therefore suggest that the physiological bursting dynamics of a population of beta-cells is cooperatively regulated, even under intercellular communication defects induced by dis-functional channels of single-cells.
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