Acute pain is a warning signal to a living organism to prevent tissue damage produced by chemical or physical stimuli of potentially damaging intensity. In contrast to other sensory organs, the receptors for pain perception sensitize, i.e. the threshold of the stimulus for inducing pain decreases after repeated application. Sensitization of primary nociceptors is likely the major mechanism involved in chronic pain that represents the most frequent suffering and medical, ethical and economical problem.

The goal of our research is to understand the physiological significance of a specific subclass of ion channels that are involved in the detection of noxious thermal, mechanical and chemical stimuli. These channels are specifically expressed in primary nociceptive neurones and work in concert to detect potentially damaging stimuli and transduce them into pain signalling. Particularly, we investigate molecular mechanisms of nociception and thermosensation by focusing on transient receptor potential (TRP) ion channels.