The O₂ sensitivity of dissociated type I cells from rat carotid body (CB) increases with age until ~14-16 days. Hypoxia-induced depolarization appears to be mediated by an O₂-sensitive K⁺ currents, but other K⁺ currents may modulate depolarization. We hypothesized that membrane potential may be stabilized in newborn type I cells by HERG-like K⁺ currents that inhibit hypoxia-induced depolarization, and that a decrease in this current with age could underlie, in part, the developmental increase in type I cell depolarization response to hypoxia. In dissociated type I cells from 0-1 day and 11-16 day old rats, using perforated patch-clamp and 70 mM K⁺ extracellular solution, repolarization-induced inward K⁺ tail currents were measured in the absence and presence of E-4031, a specific HERG channel blocker. This allowed isolation of the E-4031-sensitive HERG-like current. E-4031-sensitive peak currents in type I cells from 0-1 day were 2.5 fold larger than in cells from 11-16 day old rats. E-4031-sensitive current density in newborn type I cells was 2 fold greater than in cells from 11-16 days. Under current clamp conditions, E-4031 enhanced hypoxia-induced depolarization in type I cells from 0-1 day but not 11-16 day old rats. Using Fura-2 to measure intracellular calcium, E-4031 increased the [Ca²⁺]_i response to anoxia in cells from 0-1 day but not cells from 11-16 day old rats. E-4031-sensitive K⁺ currents are present in newborn CB type I cells and decline with age. These findings are consistent with a role for E-4031-sensitive potassium current, and possibly HERG-like potassium currents, in the type I cell hypoxia response maturation.