1. In current and voltage clamp, the effects of hypoxia were studied o
n resting and synaptic properties of hypoglossal motoneurones in barbi
turate-anaesthetized adult cats. 2. Twenty-nine hypoglossal motoneuron
es with a mean membrane potential of -55 mV responded rapidly to acute
hypoxia with a persistent membrane depolarization of about +17 mV. Th
is depolarization correlated with the development of a persistent inwa
rd current of 0.3 nA at holding potentials close to resting membrane p
otential. 3. Superior laryngeal nerve (SLN) stimulation-evoked EPSPs w
ere reduced in amplitude by, on average, 46%, while IPSP amplitude was
reduced by 31%. SLN stimulation-evoked EPSCs were reduced by 50-70%.
4. Extracellular application of adenosine (10 mM) hyperpolarized hypog
lossal motoneurones by, on average, 5.6 mV, from a control value of -6
2 mV. SLN stimulation-evoked EPSPs decreased by 18% and IPSPs decrease
d by 46% during adenosine application. 5. Extracellular application of
the K-ATP channel blocker glibenclamide led to a blockade of a persis
tent outward current and a significant increase of SLN stimulation-evo
ked EPSCs. 6. We conclude that hypoglossal motoneurones have a very lo
w tolerance to hypoxia. They appear to be under metabolic stress even
in normoxia and their capacity to activate protective potassium curren
ts is limited when compared with other brainstem neurones. This may he
lp to explain the rapid disturbance of hypoglossal function during ene
rgy depletion.