Neuropathic pain is a complex
chronic pain state caused by the dysfunction of somatosensory nervous system, and it affects the millions of people worldwide. At present, there are very few medical treatments available for
neuropathic pain management and the intolerable side effects of medications may further worsen the symptoms. Despite the presence of profound knowledge that delineates the pathophysiology and mechanisms leading to
neuropathic pain, the unmet clinical needs demand more research in this field that would ultimately assist to ameliorate the
pain conditions. Efforts are being made globally to explore and understand the basic molecular mechanisms responsible for somatosensory dysfunction in preclinical
pain models. The present review highlights some of the novel molecular targets like
D-amino acid oxidase, endoplasmic reticulum stress
receptors, sigma receptors, hyperpolarization-activated
cyclic nucleotide-gated cation channels,
histone deacetylase, Wnt/β-
catenin and Wnt/Ryk,
ephrins and
Eph receptor tyrosine kinase, Cdh-1 and mitochondrial
ATPase that are implicated in the induction of
neuropathic pain. Studies conducted on the different animal models and observed results have been summarized with an aim to facilitate the efforts made in the drug discovery. The diligent analysis and exploitation of these targets may help in the identification of some promising
therapies that can better manage
neuropathic pain and improve the health of patients.