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Get to the root of neuropathic pain with high-quality, reliable research products, including recombinant monoclonal antibodies, bioactive proteins, and SimpleStep® ELISA kits.
Published February 1, 2021
Neuropathic pain is a chronic pain caused by a lesion or disease of the somatosensory system, including peripheral fibers and central neurons, affecting 7-10% of the general population1. Many factors are implicated in the development of neuropathic pain, such as imbalances between excitatory and inhibitory somatosensory signaling, alterations in ion channels, and variability in the modulation of pain messages in the central nervous system1.
Numerous diseases may cause neuropathic pain, including autoimmune diseases (eg, multiple sclerosis), neurodegenerative diseases (eg, Parkinson’s disease), metabolic diseases (eg, diabetic neuropathy), infection, vascular disease (stroke), trauma, and cancer.
The immune system and inflammatory response appear to play a crucial role in the mediation of neuropathic pain. Many diverse causes of neuropathic pain (eg, spinal cord injury) are linked to excessive inflammation in both the peripheral and central nervous system, which may contribute to both the initiation and maintenance of persistent pain.
Elevated pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-6, and IL-17, are associated with neuropathic pain. They have been found to increase in animal models of neuropathic pain and the cerebrospinal fluid (CSF) and blood of patients with chronic neuropathic pain. Furthermore, both animal models and clinical studies showed that pharmacologically lowering pro-inflammatory cytokines' levels may reduce pain.
TNF-α has been widely studied in neuropathic pain, and several TNF-α inhibitors are currently FDA-approved for painful disorders, including inflammatory bowel disease and rheumatoid arthritis. However, randomized clinical trials have failed to establish the clinical efficacy of TNF-α inhibitors in neuropathic pain, despite the promising early studies.
In contrast to pro-inflammatory cytokines, anti-inflammatory cytokines, such as IL-4, IL-10, TGF-β, are linked to downregulation of the immune system and neuropathic pain relief11. Reduced levels of anti-inflammatory cytokines have been found in patients with chronic neuropathic pain conditions. Although anti-inflammatory cytokines offer an exciting new therapeutic opportunity for neuropathic pain, the current scientific evidence is limited to in vitro and animal studies.
Neuroinflammation, characterized by glial cell activation, leukocyte infiltration, and the production of inflammatory mediators, has been suggested to play a crucial role in the induction and maintenance of different types of chronic pain, including neuropathic pain. Several emerging targets have been shown to contribute to neuroinflammation and chronic pain sensitization by regulating neuron-glia interactions in the spinal cord. This includes chemokines (CXCL1, CCL2, and CX3CL1), proteases (MMP9, cathepsin S, and caspase 6), and the WNT signaling pathway.
Nociceptive neurons serve as mediators in painful stimulus transmission between the central and peripheral nervous systems. These neurons express various receptors and ion channels that can detect and process noxious stimuli, including pain signals2.
Several studies indicate that dysregulation of neurotransmitters and over-excitation of ion channels responsible for signal transmission may contribute to the sensation of neuropathic pain3,4. Also, current first-line pharmacological treatments against neuropathic pain, such as antidepressants and anticonvulsants, target specific neurotransmitter receptors and ion channels5.
The transient receptor potential (TRP) ion channels belong to the most important ion channel family that detects and transmits noxious stimuli. TRP family includes conserved nonselective calcium-permeable channels that act as molecular sensors of multiple stimuli, such as pH changes, chemical agents, temperature, and osmolarity2.
Several TRP ion channels, including TRPV1, TRPV4, and TRPM8, have been linked to neuropathic pain conditions in animal models. For example, pharmacological inhibition of TRPV1 was shown to decrease pain in several animal models of neuropathic pain6,7, while activation of the TRPM8 channel can generate analgesia in chronic neuropathic pain in rats8.
Several types of voltage-gated sodium channels (including NaV1.3, NaV1.7, NaV1.8) may be involved in neuropathic pain as their expression is changed during neuropathic pain, and their block shows therapeutic utility9. These channels are found in the dorsal root ganglion cells and therefore are likely involved in action potential generation and conduction in nociceptors. However, the specific contribution of each of those sodium channels to neuropathic pain remains unclear9,10.
To help you identify the best tools for your neuropathic pain research, we’ve compiled a list of our high-quality antibodies, proteins, and SimpleStep® ELISA kits for the key targets in neuropathic pain.
Here we recommend our specific monoclonal antibodies for key targets in neuropathic pain research, including TRP and sodium ion channels. Our neuropathic pain portfolio includes many recombinant monoclonal RabMAb® antibodies that give you the highest level of batch-to-batch consistency, unrivaled reproducibility, confirmed specificity, and a guaranteed long-term supply.
Transient Receptor Potential (TRP)
Transient receptor potential cation channel subfamily V member 1
WB, IHC-Fr, ICC/IF, Flow Cyt
Transient receptor potential cation channel subfamily V member 4
Transient receptor potential cation channel subfamily M member 8
NaV1.7 (Sodium channel protein type 9 subunit alpha)
Mouse, Rat, Human
IHC-P, Flow Cyt
NaV1.8 (Sodium channel protein type 10 subunit alpha)
Mouse, Rat, Human, Monkey
WB, IHC-P, Flow Cyt
P2X purinoceptor 7
Flow Cyt, IHC-Fr
Glutamate receptor ionotropic, NMDA 2B, GluN2B
Mouse, Rat, Human
WB, IHC-P, IP
Mu-type opioid receptor, M-OR-1
Mouse, Rat, Human
Na+ channel blocker
Brilliant Blue G
non-competitive P2X7 antagonist
GluN2B (formerly NR2B)-preferring NMDA antagonist
TRPV1 receptor antagonist
Changes in neuropeptide synthesis and release have been linked to the pain symptoms that follow chronic inflammation and neuropathic injuries. Find the right tools to investigate the role of neuropeptides in neuropathic pain.
Protachykinin-1 (cleaved into Substance P)
Calcitonin gene-related peptide 1 (CGRP)
In the table below, you can find all the research tools that you need to trace key inflammatory markers and growth factors in neuropathic pain, including reliable recombinant monoclonal antibodies, quick SimpleStep ELISA kits, and high-quality bioactive proteins.
Did you know that our highly sensitive SimpleStep ELISA kits allow you to achieve reliable results within 90 minutes, with just one wash step?
Recombinant RabMAb antibodies
SimpleStep ELISA kits
Tumor necrosis factor alpha
Transcription factor p65 (NFkB)
Brain-derived neurotrophic factor
Growth-regulated alpha protein (C-X-C motif chemokine 1)
C-C motif chemokine 2 (MCP-1)
C-C motif chemokine 5 (RANTES)
For multiplex quantification of protein biomarkers, our FirePlex®-96 immunoassay panels offer a fast, easy, and cost-effective tool to analyze large numbers of samples rapidly.
Do you study the involvement of microglia or astrocytes in the pathogenesis of neuropathic pain? Get reliable and reproducible results with our recombinant monoclonal antibodies to key cellular and neuronal markers.
Recombinant RabMAb antibodies
Peripherin (predominant in the peripheral nervous system)
Neurofilament heavy polypeptide (NF200)
Tubulin beta-3 chain (beta III Tubulin)
RNA binding protein fox-1 homolog 3 (NeuN)
Integrin alpha-M (CD11b)
Scavenger receptor cysteine-rich type 1 protein M130 (CD163)
Adhesion G protein-coupled receptor E1 (F4/80)
Calcium-binding adapter molecule 1
Mitogen-activated protein kinase 11 (p38 MAPK)
C-C chemokine receptor type 2
Glial fibrillary acidic protein
Gap junction alpha-1 protein (Connexin-43, Cx43)
Mitogen-activated protein kinase 8 (c-Jun N-terminal kinase 1, JNK1)