The molecule GABA is one of the key inhibitors of brain activity that prevents overexcitation associated with disease states such as epilepsy. However, it has been shown that in some circumstances, too much stimulation of GABA producing neurons can also paradoxically lead to disease-causing excitation. Here we employ a computational strategy, to tease out the individual contributions of subcellular processes that contribute to GABA dependent overexcitation. The computational model reproduces the phenomenon of GABA dependent excitation and simulations predict plausible mechanisms of an ostensible trigger of common disorders of excitability. The model is also a tool that future studies may employ to investigate additional disease mechanisms stemming from disruptions in the maintenance of ion homeostasis.
