Slowly adapting, but not rapidly adapting, mechanoreceptors are particularly sensitive to thermal stimulation (Iggo, 1969). Increased spontaneous activity was observed to thermal cooling in the range 40 – 17 degrees Celsius, and depressed by warming. In order to study what mechanisms may underlie thermal sensitivity, we tested a range of transient receptor potential (TRP) channel agonists and antagonists. A total of 22 adult albino Wistar-derived rats (mean weight 444 g) were used. Briefly, each animal was deeply anaesthetized with intraperitoneal urethane (2 g/kg), and then killed with urethane injected into the heart. The whisker pads were then removed from each side of the face, and individual sinus hair follicles with hair and nerve attached were microdissected out and placed in carbogenated (with bubbled medical 95% oxygen, 5% carbon dioxide) synthetic interstitial fluid (SIF) (Bretag, 1969). After slitting a follicle lengthways, it was fixed with insect pins onto a silicone elastomer Sylgard platform in a custom-made tissue bath. The follicle was pinned open to allow easy access of drugs to mechanoreceptors within the capsule. Approximately 10 mm length of the deep vibrissal nerve was kept attached, was stripped of its outer sheath, and the nerve bundle repeatedly divided and fine nerve strands teased onto a silver recording wire. Single unit recordings from mechanoreceptors were then made. Drugs were made up in SIF and applied at the rate of 1 ml/min. Drug effects were tested by comparison with control using t tests, where ** indicates P < 0.01. Of 43 units studied, 27 responded to cooling by increased spontaneous firing. The thermoTRP agonist icilin 30 – 100 µM increased spontaneous firing in these units, in a dos-dependent manner (N = 17, r = .738, P = .001). TRPM8 channel agonist, (-) menthol 200 µM, had mixed effects on spontaneous firing but consistently enhanced cold responses (121%** of control). Other TRP agonists, cinnamaldehyde 1 – 2 mM and camphor 0.5 – 2 mM, significantly reduced spontaneous activity (45% and 2%** respectively). TRPA1 agonist allyl isothiocyanate (mustard oil) 50 – 100 µM and TRPV1 agonist capsaicin 1 – 3 µM had no effect. Broad spectrum TRP antagonist, ruthenium red 30 µM, had no effect or was slightly excitatory. The TRPM8 antagonist, capsazepine 100 – 200 µM, blocked cold evoked responses (15%**). The results are consistent with the involvement of TRPM8 channels mediating the increased spontaneous firing during cooling.