Naloxone (0.1–2.0 mg/kg i.v.) increased the amplitude of both monosynaptic and polysynaptic reflexes in previously untreated acute spinal cats. The reflex enhancement was not secondary to an increase in the number of afferent fibres activated by the stimuli, nor was there evidence based on the effects of naloxone on pre- or postsynaptic inhibition that the reflex enhancement was secondary to decreased tonic inhibition of motor neurones. The observation that reflexes were enhanced in cats four to five weeks following spinal section indicated that the actions of naloxone were independent of tracts descending to the lumbar cord. The reflex enhancement produced by naloxone appears to reflect its actions as an opioid antagonist, since both morphine and oxymorphone depressed reflexes. It is suggested that the action of naloxone may be due to antagonism of an endogenous opioid.