The carotid body (CB), a small neural crest-derived paired organ located at the carotid bifurcation, is a principal component of the homeostatic acute oxygen (O₂) sensing system required to activate the brainstem respiratory center to produce hyperventilation during hypoxemia (e.g. in high altitude residents or in patients with chronic obstructive pulmonary diseases) (Weir et al. 2005). The CB parenchyma is organized in glomeruli, clusters of cells in close contact with a profuse network of capillaries and afferent sensory fibers joining the glossopharyngeal nerve. The most abundant cell types in the CB glomeruli are the neuron-like, glomus or type I cells, which are enveloped by processes of glia-like, sustentacular type II cells. Glomus cells are physiologically complex, as they are electrically excitable and express a broad variety of voltage- and ligand-gated ion channels, as well as TRP and background K⁺ channels. These cells behave as presynaptic-like elements that establish contact with the postsynaptic sensory nerve fibers. Glomus cells are arterial chemoreceptors, activated by hypoxia, hypercapnia and extracellular acidosis. Recently, it has been shown that, as suggested by experiments in vivo (Alvarez-Buylla & Alvarez-Buylla, 1988; Koyama et al. 2000), glomus cells in vitro are glucose sensors, releasing transmitters in response to hypoglycemia (Pardal & Lopez-Barneo, 2002; Garcia-Fernandez et al. 2007). Hypoxia and hypoglycemia are additive stimuli that appear to activate cell secretion through separate pathways converging on cell depolarization and extracellular Ca²⁺ influx. Responsiveness to hypoxia seems to depend on inhibition of voltage-gated K⁺ channels (Weir et al. 2005), whereas sensitivity to hypoglycemia depends on activation of a non-selective cationic conductance (Garcia-Fernandez et al. 2007). Besides its sensitivity to acute hypoxia, the CB also exhibits a well-known adaptive hypertrophic response to chronic hypoxemia, whose underlying mechanisms are poorly known. We have investigated whether adult CB growth in chronic hypoxia is due to the activation of a population of resident stem cells. Exposure of mice to a hypoxic (10% O₂ tension) isobaric atmosphere for three weeks induced a marked CB enlargement (~2-3 fold) caused by dilation and multiplication of blood vessels as well as expansion of the parenchyma, with increased number of tyrosine hydroxylase positive glomus cell clusters. Although some glomus cells can enter a mitotic cycle in response to hypoxia, the de novo production of CB glomus cells mainly depends on a population of stem cells, which form multipotent and self-renewing colonies in vitro. Cell fate mapping experiments in vivo indicate that, unexpectedly, CB stem cells are the glia-like sustentacular cells (Pardal et al. 2007). CB stem cells can be identified using glial markers such as the glial fibrillary acidic protein. Quite remarkably, the newly formed glomus cells have the same complex chemosensory properties as mature glomus cells in situ. They contain voltage-gated Ca²⁺ and K⁺ channels, are highly dopaminergic, and secrete neurotransmitters on exposure to acute hypoxia and hypoglycemia. These cells are also producers of glial cell line-derived neurotrophic factor (Pardal et al. 2007). Induction of CB growth in sustained hypoxia seems to depend, at least in part, on factors possibly produced by glomus cells and the neighbouring vascular tissue. These observations suggest that CB glomus cells are polymodal chemoreceptors with an important role in oxygen and glucose homeostasis. They also indicate that the mammalian CB is a neurogenic niche with a recognizable physiological function in adult life. CB stem cells may explain the origin of some tumours in humans (e.g. paragangliomas) and they could also be potentially useful for antiparkinsonian cell therapy.