Phenotypic changes in dorsal root ganglion and spinal cord in the collagen antibody-induced arthritis model

Background The mechanisms underlying fibromyalgia (FM) pain are not understood. The US Food and Drug Administration has recommended three drugs for treating FM—namely, pregabalin, duloxetine and milnacipran; however, these medications are associated with severe side effects. Objective To create a mouse model of FM pain using dual injections of acidic saline to cause mechanical hyperalgesia and test whether ASIC3, Nav1.7 and Nav1.8 are involved in this process and whether electroacupuncture (EA) can reverse these phenomena. Methods The FM model was established by injecting acidic saline twice into 40 ICR mice. The mice were assigned to subgroups (n=8 each) treated with different EA frequencies (2, 15 and 50 Hz). ASIC3, Nav1.7 and Nav1.8 expression levels were measured by Western blotting and immunohistochemistry. Results Significant mechanical hyperalgesia was induced on day 8 in FM mice, which was reversed by 2, 15 and 50 Hz EA. ASIC3, Nav1.7 and Nav1.8 protein levels increased significantly in both the dorsal root ganglion and in the spinal cord of FM model mice. These changes were further attenuated by 2, 15 and 50 Hz EA. Conclusion Reduced nociceptive ASIC3, Nav1.7 and Nav1.8 proteins are involved in the preventive effects of EA against FM, and this series of molecules may represent targets for FM treatment.

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Dorsal root ganglion stimulation lead fractures: potential mechanisms and ways to avoid

BMJ Case Reports ◽

10.1136/bcr-2020-241353 ◽

2021 ◽

Vol 14 (5) ◽

pp. e241353

Author(s):

Gaurav Chauhan ◽

Brandon I Roth ◽

Nagy Mekhail

Keyword(s):

Spinal Cord ◽

Chronic Pain ◽

Case Report ◽

Dorsal Root Ganglion ◽

Dorsal Root ◽

Unusual Case ◽

Pain Syndrome ◽

Structural Instability ◽

Probable Mechanism ◽

Lead Fracture

Dorsal root ganglion stimulation (DRGS) therapy is a rapidly emerging tool being used by pain physicians in the treatment of chronic pain. Complex regional pain syndrome (CRPS), a debilitating disease whose mechanism is still has yet to be fully elucidated, is a common pathology targeted by DRGS therapy, often better results than traditional spinal cord stimulation. DRGS therapy, however, is not bereft of complications. Lead migration and fracture are two examples in particular that are among the most common of these complications. The authors report an unusual case of lost efficacy due to lead fractures in patients with CRPS treated with DRGS. The case report narrates identification, management and probable mechanism of DRGS lead fracture. The structural instability of DRGS leads can yield distressing symptoms at any point during the therapy, and physicians should be cognisant of the complications of DRGS therapy.

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The N-methyl-D-aspartate (NMDA) receptor in skin, dorsal root ganglion and spinal cord: an ideal target gene for RNA interference therapy for pain relief

Neuropsychiatry ◽

10.4172/neuropsychiatry.1000209 ◽

2017 ◽

Vol 07 (03) ◽

Author(s):

Chia Chih Alex Tseng ◽

Yuan Yi Chia ◽

Chien Cheng Liu ◽

Kuan Ming Feng ◽

Ping Heng Tan

Keyword(s):

Spinal Cord ◽

Rna Interference ◽

Nmda Receptor ◽

Pain Relief ◽

Dorsal Root Ganglion ◽

Dorsal Root ◽

Target Gene

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Microglial BDNF, PI3K, and p-ERK in the Spinal Cord Are Suppressed by Pulsed Radiofrequency on Dorsal Root Ganglion to Ease SNI-Induced Neuropathic Pain in Rats

Pain Research and Management ◽

10.1155/2019/5948686 ◽

2019 ◽

Vol 2019 ◽

pp. 1-15 ◽

Cited By ~ 3

Author(s):

Xueru Xu ◽

Shaoxiong Fu ◽

Xiaomei Shi ◽

Rongguo Liu

Keyword(s):

Spinal Cord ◽

Neuropathic Pain ◽

Dorsal Root Ganglion ◽

Nerve Injury ◽

Calcium Binding ◽

Dorsal Root ◽

Intrathecal Injection ◽

Pulsed Radiofrequency ◽

Erk Phosphorylation ◽

Extracellular Signal

Background. Pulsed radiofrequency (PRF) on the dorsal root ganglion (DRG) has been applied to alleviate neuropathic pain effectively, yet the mechanisms underlying pain reduction owing to this treatment are not clarified completely. The activated microglia, brain-derived neurotrophic factor (BDNF), phosphatidylinositol 3-kinase (PI3K), and phosphorylated extracellular signal-regulated kinase (p-ERK) in the spinal cord were demonstrated to be involved in developing neuropathic pain. Also, it has been just known that PRF on DRG inhibits the microglial activation in nerve injury rats. Here, we aim to investigate whether PRF treatment could regulate the levels of BDNF, PI3K, and p-ERK in the spinal cord of rats with spared nerve injury (SNI) via suppressing the spinal microglia activation to ease neuropathic pain. Methods. The rats with SNI were intrathecally treated with minocycline (specific microglia inhibitor) or same volume of dimethyl sulfoxide once daily, beginning from 1 h before nerve transection to 7 days. PRF was applied adjacent to the L4-L5 DRG of rats with SNI at 45 V for 6 min on the seventh postoperative day, whereas the free-PRF rats were treated without PRF. The withdrawal thresholds were studied, and the spinal levels of ionized calcium-binding adapter molecule 1 (Iba1), BDNF, PI3K, and p-ERK were calculated by western blot analysis, reverse transcription-polymerase chain reaction, and immunofluorescence. Results. The paw withdrawal mechanical threshold and paw withdrawal thermal latency decreased in the ipsilateral hind paws after SNI, and the spinal levels of Iba1, BDNF, PI3K, and p-ERK increased on day 21 after SNI compared with baseline (P<0.01). An intrathecal injection of minocycline led to the reversal of SNI-induced allodynia and increase in levels of Iba1, BDNF, PI3K, and p-ERK. Withdrawal thresholds recovered partially after a single PRF treatment for 14 days, and SNI-induced microglia hyperactivity, BDNF upregulation, and PI3K and ERK phosphorylation in the spinal cord reduced on D14 due to the PRF procedure. Conclusion. Microglial BDNF, PI3K, and p-ERK in the spinal cord are suppressed by the therapy of PRF on DRG to ease SNI-induced neuropathic pain in rats.

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