The effects of morphine on the depolarizing synaptic responses produced in motoneurons by electrical stimulation of primary sensory neurones have been recorded in hemisected spinal cord preparations (8- to 12-day-old rat pups). Morphine at concentrations of 0.1-20 microM reduced a slow, long-lasting (latency greater than 1 s, duration up to 10 s) component of the ventral root potential (VRP) evoked by C-fibre strength stimulation of the dorsal root. At 2 microM the reduction in area of this slow synaptic potential was 71.7 +/- 0.9% of control values (n = 15). The earliest components of the C-fibre strength VRP (the first 100 ms) and the responses to A beta strength stimuli were unaffected by the opioid even at 10-20 microM. The intermediate, NMDA receptor antagonist (D-AP5, 40 microM)-sensitive component (which lasts 100-1000 ms) was reduced by 34 +/- 2.2% of control (n = 15), which was significantly less than the reduction of the later NMDA-independent component (P < 0.001). Morphine (0.1-20 microM) also depressed the cumulative depolarization generated by the temporal summation of synaptic responses evoked by brief trains of C-fibre strength stimuli (1 or 10 Hz). A significantly greater reduction at the lower frequency of stimulation (56.3 +/- 2.0%) than at the higher (20.3 +/- 1.69%, n = 10, measured at 2 microM morphine) was found (P < 0.005). The effects of morphine were reversible upon wash-out or superfusion with the opioid receptor antagonist naloxone (2 microM).(ABSTRACT TRUNCATED AT 250 WORDS)