Rodent models of nerve injury-induced neuropathic pain (NP) typically employ injury to the sciatic nerve and/or its branches. Studies using these models have provided pioneering mechanistic data about the drivers of peripheral nerve regeneration and the causes of NP. It however remains largely unclear what contribution collateral sprouting of afferents plays to the development of NP. To address this, we have been using an adapted version of the spared dermatome model of collateral sprouting. This model was developed by Jack Diamond and colleagues in the 1980s to induce collateral sprouting of sensory neurons anatomically isolated from the injured neurons (sprouting neurons are in separate ganglia to the injured ones) - an approach that is not feasible using standard sciatic nerve models. Using this model, they discovered that collateral sprouting is neurotrophically distinct to axon regeneration: Collateral sprouting is dependent on NGF, whereas regeneration of injured axons could proceed even in the presence of NGF blockade. We have been assessing the utility of Jack Diamond’s spared dermatome model in the study of neuropathic pain. We present data comparing the relative contribution of collateral sprouting and regeneration to hot, cold and mechanical hypersensitivity, hyperalgesia and allodynia.