Glycine and GABAA receptor‐mediated synaptic transmission in rat substantia gelatinosa: inhibition by μ‐opioid and GABAB agonists

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Abstract
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 μm) but was insensitive to bicuculline (10 μm), TTX (0.5 μm), [D-Ala2, N-Me-Phe4, Gly5-ol]-enkephalin (DAMGO, 1 μm) or baclofen (30 μm). The single-channel conductance underlying the noise was estimated to be 21 pS. 4 The μ-opioid agonist DAMGO (1-10 μm) reduced the amplitude of the evoked glycine receptor-mediated IPSC and the evoked GABAA receptor-mediated IPSC. The μ-opioid antagonist D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP, 1 μm) reversed the DAMGO inhibition. 5 The GABAB agonist baclofen (30 μm) 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 μm). 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.