  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 $\sim100\%$ 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.
