Articles: neuralgia.
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Hyperbaric oxygen (HBO) therapy is proven to attenuate neuropathic pain in rodents. The goal of the present study was to determine the potential involvement of the Kindlin-1/Wnt-10a signaling pathway during astrocyte activation and inflammation in a rodent model of neuropathic pain. ⋯ Our findings demonstrate that HBO attenuated CCI-induced rat neuropathic pain and inflammatory responses, possibly through regulation of the Kindlin-1/Wnt-10a signaling pathway.
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J Pain Symptom Manage · Dec 2017
Neuropathic pain and Nerve Growth Factor in Chemotherapy-Induced Peripheral Neuropathy: prospective clinical-pathological study.
Neuropathic pain can be present in patients developing chemotherapy-induced peripheral neuropathy (CIPN). Nerve growth factor (NGF) is trophic to small sensory fibers and regulates nociception. ⋯ Serum NGF increases in cancer patients receiving taxane or platinum with painful CIPN, suggesting that it might be a potential biomarker of the presence and severity of neuropathic pain in this population. Long-term comprehensive studies to better define the course of NGF in relation with neurological outcomes would be helpful in the further design of therapies for CIPN-related neuropathic pain.
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Hyperbaric oxygen (HBO) has the potential to relieve neuropathic pain. The purpose of this study was to determine whether the NO-cGMP-PKG signaling pathway is involved in the analgesic effects of early hyperbaric oxygen treatment of neuropathic pain in rats. ⋯ Early HBO therapy could significantly improve symptoms of hyperalgesia of neuropathic pain in rats, possibly via activation of the NO-cGMP-PKG signaling transduction pathway.
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This study explored the putative mechanisms of miRNAs in the anterior cingulate cortex (ACC) in modulation of neuropathic pain induced by chronic constriction injury (CCI) of the sciatic nerve. ⋯ Our results suggested that CCI induces lateralized adaptations of NR2B subunit expression in the ACC, which is likely in part contributed by alterations of miR-539 expression, and may promote the regulations of neuropathic pain via NR2B-containing NMDA receptor-mediated neuronal mechanisms.
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The P2Y12 receptor expressed in satellite cells of the trigeminal ganglion is thought to contribute to neuropathic pain. The functional interaction between neurons and satellite cells via P2Y12 receptors and phosphorylated extracellular signal-regulated kinase 1/2 (pERK1/2) underlying neuropathic pain in the tongue was evaluated in this study. Expression of P2Y12 receptor was enhanced in pERK1/2-immunoreactive cells encircling trigeminal ganglion neurons after lingual nerve crush. ⋯ Co-administration of 2-MeSADP + MRS2395 to naïve rats did not result in hypersensitivity of the tongue. The relative number of CGRP-immunoreactive neurons increased following this co-administration, but to a lesser degree than observed in 2-MeSADP-administrated naïve rats, and the relative number of neurons encircled by pERK1/2-immunoreactive cells did not change. These results suggest that the interaction between activated satellite cells and CGRP-immunoreactive neurons via P2Y12 receptors contributes to neuropathic pain in the tongue associated with lingual nerve injury.