neuropathic pain is a very complex clinical syndrome that results as a consequence of lesions or diseases affecting the somatosensory system. lesion of peripheral nerves, diabetes, herpes zoster virus, among others, are clinical entities that may cause neuropathic pain. neuropathic pain also reflects changes of the normal physiology of the nociceptive transmission neurons that may happen at peripheral and central levels. these mechanisms include the generation of ectopic discharges, genomic changes of the neurons involved, alterations of ionic channels and of the endogenous inhibition of pain, abnormal activation of the immune system as well as peripheral and central sensitization. this article review the molecular and neuroplastic mechanisms associated to neuropathic pain and discuss different experimental models for its study. the development of these models has been helpful to understand the subjacent mechanisms of this pathology, and has contributed to design new therapeutical approaches and the correct diagnose of the disease.