Delta and mu receptors (DOR & MOR) are differentially expressed by A- and C-nociceptors, and are hypothesised to differentially modulate mechanical and thermal nociceptive behaviours respectively1. A- and C-nociceptors can be preferentially activated by controlled contact heating2, allowing identification of the nociceptor population driving nociceptive changes, with no confound of different stimulus modalities. Neurons in the superficial dorsal horn (dh) process C-nociceptor inputs from the area of primary hyperalgesia. This is hypothesised to activate lamina I projection neurons, higher centres, and descending control pathways, which contribute to central sensitisation leading to enhanced responses of dh neurons to A-nociceptor input in secondary hyperalgesia. We hypothesised that sensitised responses to specific A- and/or C-nociceptor inputs, rather than to stimulus modalities (mechanical/thermal) are differentially controlled by MOR/DOR in inflammatory hyperalgesia. 1° & 2° inflammatory hyperalgesia were induced by injection of Freund’s Complete Adjuvant into dorsal hindpaw and knee joint respectively under brief isofluorane anaesthesia (2-4% in O2). After 7 days, animals were re-anaesthetised (halothane 2-4% in O2, alfaxan maintenance (25.mg.kg-1 i.v.)) and DAMGO (MOR agonist 12 pmol/20μl) and SNC80 (DOR agonist 120 nmol/20μl) given intrathecally in inflamed or control animals. Withdrawal thresholds were determined in response to preferential activation of C- or A-nociceptors with contact heat stimulation, and to mechanical stimulation of the hindpaw. MOR and DOR agonists both inhibited A- and C-nociceptor evoked-responses in all groups (control, 1° & 2° hyperalgesia). SNC80 had a significantly greater effect on A-nociceptor-withdrawal thresholds in 2° hyperalgesia compared to controls, and a significantly smaller effect on A-nociceptor-evoked responses on 1o hyperalgesia (control, 8.6±0.4°C.hr; 1°, 5.9±0.6°C.hr; 2°, 13.2±1.4°C.hr; AUC mean±SEM, p<0.01). DAMGO had equivalent effects on preferential A- and C-nociceptor thermal stimulation under all conditions, but significantly increased withdrawal thresholds in response to mechanical stimuli in 2o but not 1o hyperalgesia compared to controls (control, 11.6±4.5°C.hr; 2°, 35.9±9.6°C.hr; p < 0.05). SNC80 had a greater effect on mechanical stimuli than DAMGO in all animals (p<0.05), but effects were equivalent in hyperalgesic and control animals. These results suggest that both MOR and DOR can modulate both unmyelinated and myelinated nociceptive inputs. DOR may have a greater contribution to the processing of A-nociceptor inputs in thermal 1° and 2° hyperalgesia than MOR, and MOR may be more important in modulation of responses to mechanical stimulation in 2° hyperalgesia.