Animal models of neuropathic pain have been established and used intensively over the last decade, but the molecular mechanisms underlying neuropathic pain conditions are heterogeneous and not yet fully elucidated. We have used chronic constriction injury (CCI) as a model of neuropathic pain and analysed action potential (AP) waveforms and other membrane properties in isolated dorsal root ganglion (DRG) neurons from the lumbar 4 and 5 section. RESULTS: Neuron excitability, input resistance and resting membrane potential was similar in DRG neurons from CCI (ipsilateral) (n=52) versus naive (n=45) animals, neither did we observe any increase in spontaneous activity, but we saw indications of an increased AP shoulder in a subgroup of middle sized neurons (9 out of 46). Shoulder size was measured as broadness at half amplitude of the AP. The mean broadness shifted from 4.46 ±3.2 ms to 6.67 ±6.2 ms in control (n=45) versus CCI (n=46) DRG neurons. We were able to block the shoulder with the specific N-type Ca2+ channel blocker w-conotoxin MVIIA, 0.5 mM (n=6) suggesting that the N-type calcium channel is important in the formation of a shoulder on APs in L4 and L5 DRG neurons. Comparing other characteristics showed that capsaicin sensitive cells (n=48) where all small, with averaged broader action potentials (6.42 ±6.2 ms) than capsaicin insensitive cells (4.73 ±3.3 ms) (n=32). Also all the broad APs had a relatively slow upstroke during the initial depolarizing phase of the AP, indicating either fewer or slower voltage gated sodium channels in cells with broad action potentials. We hypothesize that the increased broadness in ipsilateral CCI DRG neurons is coursed by change in Ca2+ conductance mediated by N-type channels and it is happening in a subgroup of neurons in the DRG population. Electrophysiological and qPCR studies are being conducted to further validate the reported trend. (All data are means ±SD)