AbstractThe 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 μM 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 2μM 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 Aβ strength stimuli were unaffected by the opioid even at 10‐20μM. The intermediate, NMDA receptor antagonist (D‐AP5, 40μM)‐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 μM) 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 μM morphine) was found (P<0.005). The effects of morphine were reversible upon wash‐out or superfusion with the opioid receptor antagonist naloxone (2 μM). The depression in the C‐fibre‐evoked VRPs produced by the NMDA receptor antagonist D‐AP5 (10‐40 μM) was different from that produced by morphine, as D‐AP5 only reduced a shorter latency component of the VRP (100 ms‐1 s) and was equally effective in decreasing the cumulative depolarizations evoked by 1 and 10 Hz trains. The preferential effect of morphine on the longest latency and longest lasting components of the high‐threshold VRP are discussed in relatio