Task2 potassium channels set central respiratory CO₂ and O₂ sensitivity
2010
Gestreau, Christian | Heitzmann, Dirk | Thomas, Joerg | Dubreuil, Véronique | Bandulik, Sascha | Reichold, Markus | Bendahhou, Saïd | Pierson, Patricia | Sterner, Christina | Peyronnet-Roux, Julie | Benfriha, Chérif | Tegtmeier, Ines | Ehnes, Hannah | Georgieff, Michael | Lesage, Florian | Brunet, Jean-François | Goridis, Christo | Warth, Richard | Barhanin, Jacques
Task2 K⁺ channel expression in the central nervous system is surprisingly restricted to a few brainstem nuclei, including the retrotrapezoid (RTN) region. All Task2-positive RTN neurons were lost in mice bearing a Phox2b mutation that causes the human congenital central hypoventilation syndrome. In plethysmography, Task2⁻/⁻ mice showed disturbed chemosensory function with hypersensitivity to low CO₂ concentrations, leading to hyperventilation. Task2 probably is needed to stabilize the membrane potential of chemoreceptive cells. In addition, Task2⁻/⁻ mice lost the long-term hypoxia-induced respiratory decrease whereas the acute carotid-body-mediated increase was maintained. The lack of anoxia-induced respiratory depression in the isolated brainstem-spinal cord preparation suggested a central origin of the phenotype. Task2 activation by reactive oxygen species generated during hypoxia could silence RTN neurons, thus contributing to respiratory depression. These data identify Task2 as a determinant of central O₂ chemoreception and demonstrate that this phenomenon is due to the activity of a small number of neurons located at the ventral medullary surface.
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