Chemosensory Inputs and Neural Remodeling in Carotid Body and Brainstem Catecholaminergic Cells

Exposure to hypoxia elicits an immediate increase in ventilation in order to face the tissue oxygen deficit. The acute response to hypoxia develops gradually over several days despite a constant level of isocapnic hypoxia, before reaching a steady state level which has been termed ventilatory acclimatization to hypoxia (VAH). The functional acclimatization to hypoxia reveals a striking plasticity of the chemoreflex, which takes place within the first days of exposure and can be prolonged for weeks, months or years. There is clearcut evidence that the peripheral arterial chemoreceptors play a major role in initiating the ventilatory acclimatization to hypoxia. However, this does not preclude a role for central structures involved in the translation of chemosensory inputs and modulating the integration of carotid chemo-afferent inputs. Early and recent studies have shown that the ventilatory plasticity induced by sustained hypoxia is associated with changes in the morphology and phenotype of the carotid chemoreceptors, increases in neurotransmitter biosynthesis and release, modulation of neuroreceptor expression in the carotid body and increased firing rate of the carotid chemo-afferent neurons. More recent studies demonstrated that the neuroplasticity also takes place during long-term hypoxia in restricted areas of the central nervous system, which have been involved in respiratory and sympathetic responses to hypoxia. This short review is devoted to the neurochemical plasticity induced by sustained hypoxia in the carotid body and in brainstem structures involved in translation of the peripheral chemosensory inputs, and their possible role in triggering or modulating ventilatory acclimatization to hypoxia.