Cancer-induced bone pain is a major clinical problem. A rat model based on intra-tibial injection of MRMT-1 mammary tumour cells has been developed to mimic progressive cancer-induced bone pain. At the time of stable behavioural changes (decreased thresholds to mechanical and cold stimuli) and bone destruction, in vivo electrophysiology has been used to characterize natural (mechanical, thermal, and cold) and electrical-evoked responses of superficial and deep dorsal horn neurones in halothane-anaesthetized rats. Receptive fields were significantly enlarged for superficial neurones in the MRMT-1 animals and ratios of nociceptive cell types was substantially different. Populations of neurones in MRMT-1-injected rats had significantly increased responses to mechanical, thermal and other stimuli. These alterations in dorsal horn neurones have not been reported in neuropathy or inflammation adding to the evidence for cancer-induced bone pain reflecting a unique pain state. I will discuss the pharmacology of this pain model and then present data that clearly shows in animals the importance of phenotype in responses to pain and drugs.