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The TASK background K2P channels: chemo- and nutrient sensors

Authors :: Eric Honoré
Fabrice Duprat
Amanda Patel
Inger Lauritzen
Institut de pharmacologie moléculaire et cellulaire (IPMC)
Université Nice Sophia Antipolis (... - 2019) (UNS)
COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)
ANR 2005 Cardiovasculaire-obésité-diabète, Association for Information and Research on Genetic Kidney Disease France, Fondation del Duca, Fondation de France, Fondation de la Recherche Médicale, EEC Marie-Curie fellowships, Fondation de Recherche sur l'Hypertension Artérielle, AFM, HFSP,INSERM and CNRS
Source :: Trends in Neurosciences, Trends in Neurosciences, Elsevier, 2007, 30 (11), pp.573-80. ⟨10.1016/j.tins.2007.08.003⟩
Publication Year :: 2007
Publisher :: Elsevier BV, 2007.
Abstract: Specialized chemo- and nutrient-sensing cells share a common electrophysiological mechanism by transducing low O(2), high CO(2) and low glucose stimuli into a compensatory cellular response: the closing of background K(+) channels encoded by the K(2P) subunits. Inhibition of the TASK K(2P) channels by extracellular acidosis leads to an increased excitability of brainstem respiratory neurons. Moreover, hypoxic down-modulation of TASK channels is implicated in the activation of glomus cells in the carotid body. Stimulation of both types of cell leads to an enhanced ventilation and to cardiocirculatory adjustments. Differential modulation of TASK channels by acidosis and high glucose alters excitability of the hypothalamic orexin neurons, which influence arousal, food seeking and breathing. These recent results shed light on the role of TASK channels in sensing physiological stimuli.