Studying TTX-resistance in cutaneous receptive fields we discovered the phenomenon described in the title first in mechano-cold sensititve C-fibres (CMC). We extended the study including mechano-heat sensitive (CMH) and mechanosensitive fibres (CM) (obtained from humanely killed animals) using controlled electrical stimulation to assess excitability. The most sensitive spot in the receptive field (threshold current <50μA at 1ms) was electrically stimulated with a high impedance (9-12 MΩ) needle electrode and a constant-current stimulus isolator (max. 10mA) varying stimulus intensity and duration. In all fibre classes the terminals became less excitable with cooling, thus higher currents were needed to evoke action potentials, occuring at longer latencies. These effects were readily explained by the established influence of temperature on the kinetics of TTX-sensitive sodium channels (1). There was no consistent change in rheobase current; however, with cooling from 30° to 10°C strength-duration (S-D) time constant (2) increased, most distinctively in cold-sensitive units (6.2-fold ±2.8 S.E.M., n=4; other units: 1.5-fold ±0.4 S.E.M., n=11). To apply TTX (1μM) and restrict its diffusion, the receptive field was covered with a cylindrical superfusion chamber (outer diameter 15mm) sparing a small hole (1.5mm) in the bottom. All CMC-units tested were blocked at 30°C within ≤2min after TTX application; the maximal current was insufficient to evoke action potentials. Nonetheless, when cooled down to 10°C the fibres started firing below their previously established threshold temperature (15-23°C) and clearly responded to mechanical and to electrical stimulation. However, threshold currents were largely increased (2-20-fold) and latencies prolonged by 2-8% in comparison to pre-TTX-values at 10°C. The latter phenomena also occurred upon cooling in some of the CM- and CMH-fibres that had previously been blocked by TTX at 30°C. However, the majority of the CMH-fibres were blocked only after a 30-40min exposure time and increasing TTX concentration to 6-12.5μM. We suggest that the terminals cooling manoeuvre uncovered an, at least latent, capacity of nociceptive C-fibre terminals to generate action potentials in the presence of TTX. The large increase in S-D time constant during cooling (in cold-sensitive fibres) probably reflects an increase in membrane ('input') resistance such that generator potentials created by cold (3)- and mechanically activated (4) inward currents can reach the high threshold of TTX-resistant sodium channels and trigger (slowly propagated) action potentials. If these action potentials prove to rely on TTX-resistant sodium channels, our findings extend the possibilities to examine the pharmacology of TTX resistance in sensory nerve endings under physiological conditions.