Articles: neuropathic-pain.
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Neuroscience letters · Feb 2019
The involvement of iron responsive element (-) divalent metal transporter 1-mediated the spinal iron overload via CXCL10/CXCR3 pathway in neuropathic pain in rats.
Iron is pivotal for life, but it is toxic if in excess. Iron overload mediated by divalent metal transporter 1 (DMT1) in the central nervous system has participated in various neuroinflammatory diseases. Chemokine-induced neuroinflammation involves the development of pathological pain. Recently, chemokine CXCL10 is implicated in the pathogenesis of chronic pain, however, little is known about the potential link between iron accumulation and CXCL10 in pain condition. Here, we examined whether iron accumulation regulated neuropathic pain via CXCL10. ⋯ Our findings demonstrated the contribution of spinal abnormal iron accumulation in regulating CXCL10 pathway in the pathogenesis of neuropathic pain.
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Sphingosine 1-phosphate receptor 2 (S1PR2), a member of the seven-transmembrane receptor family, can be activated by its natural ligand sphingosine 1-phosphate (S1P) to initiate signal transduction and is involved in a wide range of biological effects such as immune cell migration and vascular permeability. Its relationship with neuropathic pain (NP) has not been reported. In this study, the effects of S1PR2 on the development of NP were studied. ⋯ S1PR2 deficiency could increase the pain sensitivity of a NP mouse model and promote the development of NP
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MicroRNAs have been reported to be an important pathophysiological factor in neuropathic pain. However, the potential mechanism through which miRNAs function in neuropathic pain remains unclear. The purpose of this study was to explore the potential role of mir-34c in neuropathic pain in a mouse model of chronic constriction injury (CCI). ⋯ We also demonstrated that miR-34c suppressed the expression of NLRP3 by directly binding the 3'-untranslated region. Overexpression of miR-34c decreased the protein levels of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in the spinal cord in CCI mice. Together, our results indicated that miR-34c may inhibit neuropathic pain development in CCI mice through inhibiting NLRP3-mediated neuroinflammation.
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Virtual and augmented imagery are emerging technologies with potential to reduce the severity and impact of neuropathic pain in people with spinal cord injury (SCI). ⋯ Although the number of studies and individual sample sizes are small, these initial findings are promising. Given the limited options available for the effective treatment of neuropathic SCI pain and early evidence of efficacy, they provide valuable incentive for further research.
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The physiological mechanisms behind the therapeutic effects of spinal cord stimulation (SCS) are only partially understood. Our aim was to perform a literature review of studies that used objective measures to characterize mechanisms of action of SCS in neuropathic pain patients. ⋯ SCS appears to modulate pain via spinal and/or supraspinal mechanisms of action (e.g., pain gating, descending pain inhibition). However, to better understand the mechanisms of action of SCS, we believe that it is necessary to carry out systematic, controlled, and well-powered studies using objective patient measures. To optimize the clinical effectiveness of SCS for neuropathic pain, we also believe that it is necessary to develop and implement patient-specific approaches.