In sensory neurons transmitters bind to G-protein coupled receptors (GPCR), and activate second messenger systems (IP3, DAG, PLC, PKC). Transient receptor potential (TRP) channels are Ca2+ permeable cation channels that are activated by depletion of intracellular Ca2+ stores or subsequent to PLC activation. In expression systems, GPCRs couple to TRPC channels via Gq/11 and stimulation of GPCRs is followed by increases in [Ca2+]_i. We investigated TRPC channels in DRG neurons at transcriptional (RT-PCR), translational (immuno-histochemistry) and functional (FURA-2 microfluorimetry) level. Lumbar DRG contained mRNA for six out of the seven channel subtypes known to date. TRPC1, 3 and 6 proteins could be demonstrated in sub-populations of sensory neurons. Neurons expressing vanilloid receptor 1 (TRPV1), a marker of nociceptive neurons, were also immunoreactive for TRPC1, 3 and 6. Activation of GPCRs using muscarine, trypsin or bradykinin induced increases in [Ca2+]i which depended on the presence of extracellular Ca2+. A similar influx of Ca2+ was induced by oleylacylglycerol or arachidonic acid. Rises in [Ca2+]i were inhibited in the presence of SKF96365 or blockers of protein kinase, DAG lipase, lipoxygenase and cyclooxygenase but not after depletion of intracellular Ca2+-stores by thapsigargin. Together our data suggest a possible involvement of TRPC channels in GPCR mediated Ca2+ signaling in sensory neurons.