Increased levels of CO 2 (hypercapnic acidosis, HA) acidify central CO 2 chemoreceptors resulting in a change in neuronal excitability that drives ventilation. Recently, we developed a mathematical model that combines a minimal Hodgkin‐Huxley (HH)‐based expression of neuronal excitability with a robust transport model based on the Goldman‐Hodgkin‐Katz (GHK) equation, and used this model to study excitability in response to HA. We found that HA induced small passive changes in ionic composition that modulated membrane potential ( V m ), but the firing rate changes observed were not wholly consistent to those reported in the literature, suggesting that pH‐sensitive currents may be required. Although previous HH‐based single‐compartment neuron models have been developed to investigate CO 2 chemoreception, these models contain only an estimate of pH regulatory fluxes. To overcome the limitations of the existing models, we have (1) expanded our model to include pH‐sensitive currents proposed to participate in CO 2 chemoreception and (2) identified the role of each current in modulation of V m . We found that the expanded model with kinetic descriptions for pH regulatory mechanisms, HA‐induced small passive changes in ionic composition, and pH‐sensitive currents best captures the neuronal response to HA. We suggest that all components be included in transduction models of CO 2 chemoreception. Supported by NS045321