We describe the characterization of a partial saphenous nerve injury (PSNI) model of neuropathic pain in the mouse. PSNI resulted in significant mechanical allodynia in mice with no behavioural change to temperature stimulation. PSNI also resulted in ipsilateral paw ventroflexion, reduced functional innervation of the dorsal hindpaw and increased expression in the dorsal root ganglion of the neuropeptide galanin. We have used the PSNI model to study the electrophysiological properties of injured primary afferent neurones, demonstrating that single fibres can be identified and their properties studied. In galanin knockout mice, PSNI failed to induce allodynia as previously reported in other neuropathic pain models. PSNI can be used to simultaneously study behavioural and neurophysiological changes in wild-type and transgenic mice.