In vitro superfusion release experiments and autoradiography were carried out on spinal cords of neonatally capsaicin-treated rats. Electrical and chemical stimulations significantly increased the release of aspartate, glutamate and gamma-aminobutyric acid (GABA) from hemisected dorsal horn slices of vehicle-treated animals. In capsaicin-treated rats, the evoked release of aspartate, glutamate and substance P but not GABA, were significantly lower. Capsaicin (1 microM) stimulated the release of aspartate and glutamate, as reported for substance P, in control slices but this effect was not as apparent in tissues from capsaicin-treated rats. Evoked GABA release was not affected in either case. alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), kainate, dizocilpine and GABAB binding sites were highly localised in the substantia gelatinosa. Capsaicin treatment did not affect the affinity of the binding sites in all four cases but significantly reduced the density of kainate, dizocilpine and GABAB binding sites. The data suggest that capsaicin-sensitive primary afferent fibres release aspartate, glutamate and Substance P following high-intensity stimulations and that this release might be modulated by presynaptic glutamate and GABAB receptors present on these terminals.