1. Neuronal systems activated by stimulation in the region of the locus coeruleus/subcoeruleus (LC/SC) and raphe nuclei have previously been shown to depress transmission from group II muscle afferents in regions of the midlumbar spinal segments in which premotor interneurones are located. The aim of the present investigation was to determine the extent to which such depression is paralleled by depression of the reflex actions of group II afferents on motoneurones. 2. The effects of short trains of conditioning electrical stimuli applied within the LC/SC and raphe nuclei were examined on postsynaptic potentials (PSPs) evoked by group I and group II muscle afferents in hindlimb motoneurones. The effects were examined over a wide range of conditioning-test intervals but particular emphasis was placed on the effects produced at long intervals (> 100 ms) since such effects are more likely to be mediated by the descending noradrenergic and serotonergic neurones of the LC/SC and raphe nuclei which are of slow conduction velocity. In addition, conditioning stimuli alone evoked PSPs in motoneurones (with latencies of 7-15 ms and a duration of 50-80 ms) and effects evoked at short conditioning-test intervals might therefore have been secondary to changes in motoneurone membrane properties. 3. At conditioning-test intervals between 100 and 350 ms synaptic actions of group II origin were strongly and consistently depressed. Both EPSPs and IPSPs were affected, two-thirds of those tested being reduced in amplitude by 50% or more. A similar depression was exerted on PSPs evoked from the quadriceps and deep peroneal nerves mediated predominantly by interneurones located in the midlumbar segments and on PSPs evoked from the hamstring and triceps surae nerves mediated by interneurones located in more caudal segments. It is thus concluded that neuronal systems activated by stimuli applied in the LC/SC and raphe nuclei are capable of gating transmission in all those interneuronal pathways which mediate the reflex actions of group II afferents on motoneurones in anaesthetized animals.
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