Recently, we showed that capsaicin induced the degeneration of not only glomerular CI terminals but also of non-glomerular CI terminals making presynaptic contact with interneuronal soma. Studies of the nature of interneurons making contact by nonglomerular CI terminals should provide important information to facilitate our understanding of the processing of nociceptive impulses in the substantia gelatinosa. The most likely candidate molecule involved in this process in these interneurons is gamma-aminobutylic acid (GABA). Therefore, ultrastructural relationships between nonglomerular CI terminals land GABAergic interneuronal soma in the mouse substatia gelatinosa were examined by an immunocytochemical method using an antibody to GABA. Terminals with the same profiles as the CI terminals, i.e., slender, sinuous and scalloped terminals filled with clear synaptic vesicles, were found to make synaptic contacts with GABA-immunoreactive somata. Thus, nociceptive primary afferents are suggested to modulate pain transmission by themselves via GABAergic neurons in the substantia gelatinosa.