Increased levels of CO2 (hypercapnic acidosis, HA) acidify central CO2 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 (Vm), 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 CO2 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 CO2 chemoreception and (2) identified the role of each current in modulation of Vm. 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 CO2 chemoreception. Supported by NS045321