The effects of the A1 agonist GW684067, (2R,3R,4S,5R)-5-ethynyl-2-[6-tetrahydro-2H-pyran-4-ylamino)-9H-purin-9-yl]tetrahydrofuran-3,4-diol) were assessed on the response of dorsal horn neurones sensitized by the intraplantar injection of capsaicin. Single unit recordings were made using multi-electrode arrays in the spinal cord of 12 Saffan-anaesthetized male CD rats 200-250g, from 59 neurones that responded to pinch of the hind paw receptive field (RF), recorded at depths of 444-1029 μm from the surface. Saffan was administered by intravenous perfusion (10 mg/kg/h). Each ml of Saffan contains 9 mg alfaxalone and 3 mg/kg alfadolone acetate. Baseline responses were evoked by mechanical stimulation (von Frey filaments, 1-164 g, 10s) to the RF before and after capsaicin injection (10 μg in 10μl) approximately 15 mm outside the RF. GW684067 or vehicle (saline) was administered either i.v. (0.1 mg/kg) or topically to the spinal cord (1.5 μg in 150 μl) immediately after capsaicin injection. Mechanical stimulation was continued every 15 min for 75 min. Counts of action potentials per stimulus were analysed by Student′s paired t test. Capsaicin caused a significant enhancement of responses to 164 g von Frey stimulation; following vehicle administration either topically or i.v., responses were increased by 414 ± 133% (n=16, 3 rats) and 307 ± 84% (n=14, 3 rats), respectively (mean ± s.e.m; P<0.05 vs pre-capsaicin control). In contrast, in the presence of GW684067 administered topically to the spinal cord, capsaicin inhibited any sensitisation compared to vehicle or baseline (29 ± 10% decrease compared to baseline, P<0.02, n=13, 3 rats). GW684067 i.v. also significantly reduced the sensitisation when compared to vehicle (16 ± 14% increase compared to baseline, P<0.02 vs vehicle control, n=16, 3 rats). GW684067 significantly inhibited the spontaneous firing rate of the neurones when administered either topically to the cord or i.v. (39 ± 4% and 38 ± 7% decrease; P<0.05 vs. pre-capsaicin baseline). Vehicle had no significant effect the spontaneous firing rate. These data indicate that the adenosine A1 agonist GW684067, whether administered systemically or spinally, significantly reduced both the ongoing discharge of dorsal horn neurones and the secondary hypersensitivity induced by intraplantar capsaicin.