Santosh Nagare
As we know that pain is the most common reason for which a patient takes medicine. Pain is not a single entity but may be classified as nociceptive pain, inflammatory
pain, and neuropathic pain. In this review we have exclusively Neuropathic pain is caused by the direct lesion on the neuron or damage or dysfunction of peripheral
or central neurons. Although the neuropathic pain is single entity theoretically but it involve broad arena of receptor and mediators like melanocortin and its receptor
(Type4), TLR7, TLR8, Sphingosine-1 phosphate receptor, CCL2, P2X4, and PARP-1 regulated expression of inflammatory mediator. Because of such dynamic interplay
amongst the mediators and its corresponding receptor in addition to the inflammatory ligand and its receptor even the smallest stimulation results in spontaneous intense
pain after that it gets transformed into chronic pain syndrome which is difficult to treat. In chronic pain syndrome, plastic changes occur in nociceptive neurons which
can’t be reversed by pharmacological treatment. In this review, we have discussed the core pathophysiology of neuropathic pain and advances in mediator and receptor
accompanied their consequences or interaction to sustain the neuropathic pain.
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