Articles: neuropathic-pain.
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Journal of pain research · Jan 2018
OnabotulinumtoxinA injections for atypical odontalgia: an open-label study on nine patients.
Atypical odontalgia (AO) manifests as continuous pain in the region of one or several teeth, in the absence of signs of dental pathology. Currently, there is insufficient evidence to establish treatment guidelines for AO. The aim of this study was to describe the effectiveness and safety of treatment with OnabotulinumtoxinA (OnabotA) on a series of patients with AO. ⋯ OnabotA may be a safe and effective option for the treatment of AO.
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Anticancer Agents Med Chem · Jan 2018
Oxaliplatin Regulates Chemotherapy Induced Peripheral Neuropathic Pain in the Dorsal Horn and Dorsal Root Ganglion via the Calcineurin/NFAT Pathway.
The aim of this study was to investigate the mechanism of oxaliplatin in the induction of neuropathic pain as a symptom of Chemotherapy-Induced Peripheral Neuropathy (CIPN). ⋯ It was the first time to prove that oxaliplatin-induced neuropathic pain was correlated to the activation of the CaN/NFAT pathway in our rat model. This finding can provide a new direction to explore the mechanism of oxaliplatin-induced neuropathic pain.
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Background Oxaliplatin is a third-generation chemotherapeutic agent that is commonly used to treat metastatic digestive tumors; however, one of the main limiting complications of oxaliplatin is painful peripheral neuropathy. The purpose of this study was to examine the underlying mechanisms by which mammalian target of rapamycin (mTOR) and its signal are responsible for oxaliplatin-evoked neuropathic pain. Methods Neuropathic pain was induced by intraperitoneal injection of oxaliplatin in rats. ⋯ Conclusions The data revealed specific signaling pathways leading to oxaliplatin-induced peripheral neuropathic pain, including the activation of PI3K-mTOR and pro-inflammatory cytokine signal. Inhibition of these pathways alleviates neuropathic pain. Targeting one or more of these molecular mediators may present new opportunities for treatment and management of neuropathic pain observed during chemotherapeutic application of oxaliplatin.
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Chemokines-mediated neuroinflammation in the spinal cord plays a critical role in the pathogenesis of neuropathic pain. Chemokine CXCL9, CXCL10, and CXCL11 have been identified as a same subfamily chemokine which bind to CXC chemokine receptor 3 to exert functions. Our recent work found that CXCL10 is upregulated in spinal astrocytes after spinal nerve ligation (SNL) and acts on chemokine receptor CXCR3 on neurons to contribute to central sensitization and neuropathic pain, but less is known about CXCL9 and CXCL11 in the maintenance of neuropathic pain. ⋯ In addition, intrathecal injection of CXCL9 and CXCL11 did not produce hyperalgesia or allodynia behaviors, and neither of them induced ERK activation, a marker of central sensitization. Whole-cell patch clamp recording on spinal neurons showed that CXCL9 and CXCL11 enhanced both excitatory synaptic transmission and inhibitory synaptic transmission, whereas CXCL10 only produced an increase in excitatory synaptic transmission. These results suggest that, although the expression of CXCL9 and CXCL11 are increased after SNL, they may not contribute to the maintenance of neuropathic pain.
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Emerging evidence showed that hyperpolarization-activated cation channels (HCN) participate in the development of inflammatory and neuropathic pain. However, the role of HCN2 in oxaliplatin-induced neuropathic pain remains unknown. Here, we found that HCN2 expression was upregulated in a rat model of oxaliplatin-induced neuropathic pain. ⋯ Furthermore, the underlying cellular mechanism demonstrated that ZD7288 administration restrained the enhanced activation of the neuronal calcium-calmodulin-dependent kinase II (CaMKII)/cyclic adenosine monophosphate response element-binding protein cascade after oxaliplatin administration. Moreover, pretreatment of CaMKII inhibitor KN-93 suppressed the nociceptive behaviors, as well as NR2B upregulation induced by overexpression of HCN2. In a word, HCN2 is conducive to oxaliplatin-induced neuropathic pain by activating the neuronal CaMKII/CREB cascade.