We created a single-compartment computer model of a CO₂ chemosensory neuron for Helix aspersa. We incorporated into the model two inward currents, a sodium current and a calcium current, three outward potassium (K⁺) currents, an A-type current (I_KA), a delayed rectifier (I_KDR), and a calcium-activate K⁺ current (I_KCa) and a proton conductance found in invertebrate cells (I_Proton). All of the K⁺ channels were inhibited by reduced pH. We also included pH-regulatory process to mimic the effect of the sodium-hydrogen exchanger (NHE) described in these cells during hypercapnic stimulation. The model displayed chemosensory behavior (increased spike frequency during acid stimulation), and all three K⁺ channels participated in the chemosensory response and shaped the temporal characteristics of the response to acid stimulation. pH-dependent inhibition of IKA initiated the response to CO₂, but hypercapnic inhibition of I_KDR and I_KCa affected the duration of the excitatory response to hypercapnia. The presence or absence of NHE activity altered the chemosensory response over time and demonstrated the inadvisability of effective pHi regulation in cells designed to act as chemostats for acid-base regulation. The results of the model indicate that multiple channels contribute to CO₂ chemosensitivity, but the primary sensor is probably the A-type potassium channel. Intracellular pH may be a sufficient chemosensory stimulus, but it may not be a necessary stimulus -- either pHi or pHe can be effective stimuli if chemosensory neurons express appropriate pH-sensitive channels. These general principles are applicable to all CO₂ chemosensory cells in vertebrate and invertebrate neurons.