FIGURE 1.

Proposed mechanisms of CB type-I cell hyperexcitability under chronic sustained hypoxia (CSH). The scheme depicts the main ion channels described in CB type-I cells. Acute fall in the PO₂ inhibits K⁺ conductance(s) either directly on membrane components (i.e., KO₂) or indirectly by reducing mitochondrial ATP production (‘metabolic hypothesis’) triggering a membrane depolarization that leads to the calcium-dependent neurotransmitters (NTs) release, initiating the chemosensory response to hypoxia. Under CSH an increased Na-current has been suggested [Nav1.1 subunit increased expression (Cáceres et al., 2007)] while a potentiated inhibition of a TASK-like K⁺-channel activity which induced a larger depolarization has been described (Ortiz et al., 2007, 2013). A major voltage-dependent calcium entry (mainly through L-type Ca-channels) is expected, which could explain the CB neurotransmitter release imbalance under CSH. Chloride channel(s) have been related with volume (Vol) and osmolarity (Osm) regulation but they would not participate in CSH mechanisms.