1. Bicuculline-sensitive and strychnine-sensitive inhibitory postsynaptic currents (IPSCs) could be evoked in neurones of the rat substantia gelatinosa of the spinal trigeminal nucleus pars caudalis. 2. Spontaneous tetrodotoxin (TTX)-insensitive-mediated miniature IPSCs (mIPSCs) blocked by strychnine or bicuculline were also present in many neurones. The decay of the glycine receptor-mediated mIPSCs was fitted by a single exponential, whereas the decay of the GABAA receptor-mediated mIPSCs could in some instances be fitted by a single exponential, but in other instances required two exponentials. 3. An increase in baseline current noise developed during the course of the recording. This noise was abolished by strychnine (1 microM) but was insensitive to bicuculline (10 microM), TTX (0.5 microM), [D-Ala2,N-Me-Phe4,Gly5-ol]-enkephalin (DAMGO, 1 microM) or baclofen (30 microM). The single-channel conductance underlying the noise was estimated to be 21 pS. 4. The mu-opioid agonist DAMGO (1-10 microM) reduced the amplitude of the evoked glycine receptor-mediated IPSC and the evoked GABAA receptor-mediated IPSC. The mu-opioid antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 1 microM) reversed the DAMGO inhibition. 5. The GABAB agonist baclofen (30 microM) reduced the amplitude of the evoked glycine receptor-mediated IPSC and the GABAA receptor-mediated IPSC. The inhibition was reversed by the selective GABAB antagonist 3-N[1-(S)-(3,4-dichlorophenyl)ethyl]amino- 2-(S)-hydroxypropyl-P-benzyl-phosphinic acid (CGP 55845A, 1 microM). 6. Both DAMGO and baclofen reduced the frequency of glycine and GABAA receptor-mediated mIPSCs without affecting average amplitude, and increased the percentage of failures of the evoked glycine and GABAA receptor-mediated IPSCs, suggesting a presynaptic site of action.