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  • 1
    In current and voltage clamp, the effects of hypoxia were studied on resting and synaptic properties of hypoglossal motoneurones in barbiturate-anaesthetized adult cats.
  • 2
    Twenty-nine hypoglossal motoneurones with a mean membrane potential of −55 mV responded rapidly to acute hypoxia with a persistent membrane depolarization of about +17 mV. This depolarization correlated with the development of a persistent inward current of 0.3 nA at holding potentials close to resting membrane potential.
  • 3
    Superior laryngeal nerve (SLN) stimulation-evoked EPSUPs were reduced in amplitude by, on average, 46%, while IPSUP amplitude was reduced by 31 %. SLN stimulation-evoked EPSCs were reduced by 50–70%.
  • 4
    Extracellular application of adenosine (10 mm) hyperpolarized hypoglossal motoneurones by, on average, 5.6 mV, from a control value of –62 mV. SLN stimulation-evoked EPSUPs decreased by 18% and IPSUPs decreased by 46% during adenosine application.
  • 5
    Extracellular application of the KATP channel blocker glibenclamide led to a blockade of a persistent outward current and a significant increase of SLN stimulation-evoked EPSCs.
  • 6
    We conclude that hypoglossal motoneurones have a very low tolerance to hypoxia. They appear to be under metabolic stress even in normoxia and their capacity to activate protective potassium currents is limited when compared with other brainstem neurones. This may help to explain the rapid disturbance of hypoglossal function during energy depletion.