Although the central nervous system is composed of neurons with variable electrophysiological phenotypes, several groups of cells show qualitative similarities in their electrical behavior. For example, pacemaker neurons such as dopaminergic and serotoninergic neurons are spontaneously active in vitro and exhibit two distinguished firing pattern in vivo, namely single-spike and burst firing. Importantly, the firing pattern of these cells strongly affects behavioral parameters, through the modulation of neurotransmitter release. Therefore, the understanding of the mechanisms underlying this switch of firing pattern may be of critical interest. It has been shown that the blockade of small-conductance calcium-activated potassium (SK) channels has a common effect on the firing pattern of these cells, as well as many others (e.g. GnRH neurons, deep cerebellar nucleus neurons, subthalamic nucleus neurons, mitral cells of the olfactory bulb), increasing irregularity and/or bursting. On the basis of these experimental results, we have developed a minimal computational model that is general enough to apply to different types of neurons without including their specific details. Its two main components are I) the dynamics of generation of action potentials, sustained by sodium and delayed-rectifier potassium channels II) the calcium dynamics, involving L-type calcium channels and calcium pumps. In addition, stochastic activation of excitatory synaptic inputs is used to model the afferences. Using this model, we propose a common mechanism which may underlie both the control of neuronal firing and synchrony of pacemaker cells. We propose that SK channels, which act as filters against excitatory inputs through the regulation of the calcium balance in the cell, act as "isolators" against synaptically-induced bursting, and oppose the emergence of a collective rhythm entrained by a common synaptic input.