Carotid body chemoreceptors respond to a decrease in arterial partial pressure of O(2) with an increase in sinus nerve action potential (AP) activity which initiates a number of protective reflexes. The spike generation process is unresolved but is generally considered to be caused by a synaptic depolarizing potential (SDP) in the nerve endings caused by release of an excitatory transmitter from the glomus cell, which is a secretory cell that is presynaptic to the nerve terminals. To detect the purported SDPs, stimulating electrodes were placed at sites within the carotid body from which orthodromic APs could be evoked at low threshold currents. The probability of AP generation as a function of stimulus current was fitted well to a Boltzmann distribution. Subthreshold electrical stimuli which were expected to summate with subthreshold SDPs, failed, in all instances, to evoke APs at the expected probability. When the stimulus was gated to the occurrence of a spontaneous AP, no change in electrical threshold was observed as the delay between the spontaneous AP and electrical stimulus was increased, despite the presumed disappearance of an SDP in the post-AP period. Decreases in spontaneous AP generation rate, caused by hyperoxia, were associated with only slight changes in the mean orthodromic stimulus threshold, but with a significant increase in slope of the Boltzmann function, suggesting a decrease in the variance of nerve terminal excitability during hyperoxia. These results suggest that AP generation is not due to SDP events; rather, AP generation is likely to be due to a process endogenous to the nerve terminals that modulates the variability of nerve terminal excitability.