Abstract
Neuropathic pain is a debilitating form of treatment resistant chronic pain and responds poorly to the clinically available therapies. Studies from animal models of neuropathic pain have led to understanding of its pathobiology which includes complex interrelated pathways leading to peripheral and central neuronal sensitization. Advancements in the elucidation of neuropathic pain mechanisms have revealed a number of key targets that have been hypothesized to modulate clinical status. The present review discusses these therapeutic targets including noradrenaline and 5-HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, neuropeptide Y, vasoactive intestinal peptide, and CGRP; pro-inflammatory cytokines; MAP kinases; PPAR γ; Na+/Ca2+ exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation-dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; endocannabinoids; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D-amino acid oxidase. The exploitation of these targets may provide effective therapeutic agents for the management of peripheral nerve injury-induced neuropathic pain.
Keywords: Endocannabinoids, MAP kinases, neuropeptides, neuropathic pain, pro-inflammatory cytokines, DRG, Hypogonadism, WAY-318068, NS1619, GABA, GDNF, Cholecystokinin, L365260, TRPM8, LY2183240, OMDM132, PPARgamma, t-PA-STOP, JNJ7777120, CK1epsilon
CNS & Neurological Disorders - Drug Targets
Title: Therapeutic Targets for the Management of Peripheral Nerve Injury- Induced Neuropathic Pain
Volume: 10 Issue: 5
Author(s): Amteshwar Singh Jaggi and Nirmal Singh
Affiliation:
Keywords: Endocannabinoids, MAP kinases, neuropeptides, neuropathic pain, pro-inflammatory cytokines, DRG, Hypogonadism, WAY-318068, NS1619, GABA, GDNF, Cholecystokinin, L365260, TRPM8, LY2183240, OMDM132, PPARgamma, t-PA-STOP, JNJ7777120, CK1epsilon
Abstract: Neuropathic pain is a debilitating form of treatment resistant chronic pain and responds poorly to the clinically available therapies. Studies from animal models of neuropathic pain have led to understanding of its pathobiology which includes complex interrelated pathways leading to peripheral and central neuronal sensitization. Advancements in the elucidation of neuropathic pain mechanisms have revealed a number of key targets that have been hypothesized to modulate clinical status. The present review discusses these therapeutic targets including noradrenaline and 5-HT reuptake inhibitors; sodium, calcium and potassium channels; inhibitory and excitatory neurotransmitters; neuropeptides including bradykinin, tachykinin, cholecystokinin, neuropeptide Y, vasoactive intestinal peptide, and CGRP; pro-inflammatory cytokines; MAP kinases; PPAR γ; Na+/Ca2+ exchanger; nitric oxide; purinergic receptors; neuronal nicotinic receptors; cation-dependent chloride transporters; oxidative stress; matrix metalloproteinase and plasminogen activators; growth factors; transient receptor potential (TRP) channels; endocannabinoids; histamine receptors; dopamine; sigma receptors, beta adrenergic receptors, endothelins, and D-amino acid oxidase. The exploitation of these targets may provide effective therapeutic agents for the management of peripheral nerve injury-induced neuropathic pain.
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Cite this article as:
Singh Jaggi Amteshwar and Singh Nirmal, Therapeutic Targets for the Management of Peripheral Nerve Injury- Induced Neuropathic Pain, CNS & Neurological Disorders - Drug Targets 2011; 10 (5) . https://dx.doi.org/10.2174/187152711796235041
DOI https://dx.doi.org/10.2174/187152711796235041 |
Print ISSN 1871-5273 |
Publisher Name Bentham Science Publisher |
Online ISSN 1996-3181 |
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