Abstract
1. Previous studies of the effects of naloxone on spinal neural responses have yielded disparate results. The reasons for this remain unclear but may relate to the diversity of animal preparations used, the route of administration of naloxone, the site and modality of the stimuli and the intensity of afferent input used. 2. A model requiring little preparative surgery compared to most other electrophysiological preparations has now been used to investigate the effects of naloxone (1, 10, 20 and 50 micrograms kg-1 I.V.) on single-motor-unit flexion reflex responses to alternating mechanical and electrical stimuli in spinalized rats, anaesthetized with alpha-chloralose. 3. Naloxone caused a dose-dependent facilitation of reflex responses to electrical stimuli delivered at intensities sufficient to activate either A fibres alone or A and C fibre afferents together. The component of the responses presumed to be due primarily to activation of C fibres was enhanced relatively more than the A fibre component. 4. Responses evoked during high-intensity mechanical pinch stimuli were not facilitated by equivalent doses of naloxone. The post-stimulus after-discharge was, however, enhanced by a similar percentage to the response to high-intensity electrical stimuli. 5. Lowering the intensity of the mechanical stimulus led to a diminished firing rate of the units during the stimulus itself. The stimulus was, nevertheless, still noxious. Naloxone was found to have a facilitatory effect on this smaller evoked response both during the pinch stimulus and during the period of after-discharge. The apparent lack of effect of naloxone during the higher intensity mechanical stimulus may be due to neurones in the polysynaptic pathway being activated at near-maximal firing rates. 6. We conclude that the ability of naloxone to facilitate spinal reflexes is not dependent on the nature of the stimulus, at least between electrical and mechanical stimuli, but is more a function of the intensity of the applied stimulus.