Neuropathic pain (NP) is a severe health problem which is further complicated by the lack of effective therapy. The search for new treatments have recently focussed on ion channel candidates; expression and activity of many ion channels relevant to pain signalling have been found to be altered following nerve injury (Markman & Dworkin, 2006). There is compelling evidence for the role of the M-type K⁺ channels in pain transmission as the membrane excitability of small nociceptive DRG neurons is tightly controlled by M channel activity (Passmore et al. 2003). To examine the importance of the M current in the development of ectopic firing produced by the neuroma, we are examining KCNQ2, KCNQ3 and KCNQ5 (M channel subunits) expression within the sciatic nerve neuroma and DRG of partial sciatic nerve ligation (PSNL) operated rats. Adult male Wistar rats were subjected to PSNL or sham surgery. Under general anesthesia with 2% isoflurane, the nerve was exposed, partially ligated and sectioned. Quantitative RT-PCR and immunocytochemistry were used to reveal changes in KCNQ expression levels in DRG and sciatic nerve neuroma 14 and 28 days following PSNL. Preliminary data suggest an increase in ipsilateral DRG KCNQ2 expression following PSNL in comparison to contralateral KCNQ2 expression. These studies seek to reveal the importance of M channel expression in the initial stages following peripheral nerve injury, both at the primary sensory neuron soma and at the site of nerve injury. This builds on investigations suggesting that KCNQ channels may be a novel analgesic target for neuropathic pain.