RESUMEN
If the genome defines the program for the operations of a cell, signaling networks execute it. These cascades of chemical, cell-biological, structural, and trafficking events span milliseconds (e.g., synaptic release) to potentially a lifetime (e.g., stabilization of dendritic spines). In principle almost every aspect of neuronal function, particularly at the synapse, depends on signaling. Thus dysfunction of these cascades, whether through mutations, local dysregulation, or infection, leads to disease. The sheer complexity of these pathways is matched by the range of diseases and the diversity of their phenotypes. In this review, we discuss how to build computational models, how these models are essential to tackle this complexity, and the benefits of using families of models at different levels of detail to understand signaling in health and disease.