This study investigated the sensitisation of different nociceptor types in cutaneous inflammation, using a non-invasive thermal ramping protocol that can selectively activate C- or A-fibre nociceptors (1, 2). As inflammation results in oedema, which can affect the thermal conductivity of skin, we validated the thermal ramping protocol in cutaneous inflammation, and then determined the contributions of C- and A-fibre nociceptors to acute and chronic primary inflammatory hyperalgesia. In acute experiments, adult male Wistar rats (280-350g) were anaesthetised with halothane (4% in O2) and maintained on Alfaxalone infusion (25mg.kg.h-1). Cutaneous inflammation was induced with subcutaneous injection of complete Freund’s adjuvant (CFA 50µl; 1mg/ml) into the dorsal surface of the hind-paw, either under terminal (acute) or recovery anaesthesia (4% isofluorane in O2; chronic). Fast (7.5°C.s-1) or slow (2.5°C.s-1) heat ramps were applied at the injection site to preferentially activate A- or C- nociceptors respectively, and surface and subcutaneous heating rates were determined. Withdrawal thresholds to A- and C-nociceptor activation (interstimulus interval 8 min) were determined before and for 3 hours after subcutaneous injection of CFA/vehicle. In chronic inflammation, oedema and nociceptive behaviour were assessed for 7 days after CFA injection. Animals were then re-anaesthetised for terminal experiments and A- and C-nociceptor withdrawal thresholds measured. Data were analysed using one way ANOVA + Bonferroni’s post tests unless otherwise specified, and are mean±SEM. Subcutaneous heating rates were equivalent in normal and inflamed skin (slow ramps: normal = 0.6±0.03oC.s-1; inflamed 0.6±0.1 oC.s-1; p>0.05, fast ramps: normal = 2.5±0.07 oC.s-1, inflamed 2.4±0.1 oC.s-1 (n=6)). Hindpaw oedema was evident after 1 hour and maintained for 7 days (paw thickness 4.3±0.1 mm; day 7, 6.3±0.2 mm, p<0.001, n=3). In acute inflammation, thresholds to both C- and A- nociceptor stimulation were lower after 1 hour (C: 53.4±0.3oC vs. 43.6±2.1oC; p<0.001: A: 56.5±0.6 oC vs. 48.5±1.7 oC; p<0.01 n=5). However, thresholds to both C- and A-nociceptor stimulation returned towards baseline values and were not significantly different at hours 2 and 3 after CFA. In chronic inflammation, behavioural withdrawal thresholds were reduced after 7 days (pre-injection: 174.7±33.1 g.mm-1; day 7: 77.6±4.8 g.mm-1. p<0.05, n=4), but in anaesthetised animals, C- and A-heat nociceptor thresholds were raised compared to naïve controls (C-nociceptors, 53.5±0.2oC vs. 56.6±0.7oC (7 day CFA), p<0.001, A-nociceptors, 55.88±0.2oC vs 57.44±0.5 oC (7 day CFA), p<0.01, unpaired t-test, n=4). Acute cutaneous inflammation results in short-term sensitisation of both A- and C-nociceptors. In contrast, sensitisation was not seen in chronic inflammation.