Carotid body (CB) chemoreceptors transduce low arterial O(2) tension into increased action potential activity on the carotid sinus nerves, which contributes to resting ventilatory drive, increased ventilatory drive in response to hypoxia, arousal responses to hypoxia during sleep, upper airway muscle activity, blood pressure control and sympathetic tone. Their sensitivity to O(2) is low in the newborn and increases during the days or weeks after birth to reach adult levels. This postnatal functional maturation of the CB O(2) response has been termed "resetting" and it occurs in every mammalian species studied to date. The O(2) environment appears to play a key role; the fetus develops in a low O(2) environment throughout gestation and initiation of CB "resetting" after birth is modulated by the large increase in arterial oxygen tension occurring at birth. Although numerous studies have reported age-related changes in various components of the O(2) transduction cascade, how the O(2) environment shapes normal CB prenatal development and postnatal "resetting" remains unknown. Viewing CB "resetting" as environment-driven (developmental) phenotypic plasticity raises important mechanistic questions that have received little attention. This review examines what is known (and not known) about mechanisms of CB functional maturation, with a focus on the role of the O(2) environment.
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