scholarly journals The expression of corticotropin-releasing factor and its receptors in the spinal cord and dorsal root ganglion in a rat model of neuropathic pain

2011 ◽  
Vol 44 (1) ◽  
pp. 60 ◽  
Author(s):  
Eun Hyun Kim ◽  
Da Hye Ryu ◽  
Sejin Hwang
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Rat Model ◽  
Dorsal Root ◽  
Corticotropin Releasing Factor

scholarly journals 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

2019 ◽  
Vol 2019 ◽  
pp. 1-15 ◽  
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.

Altered tachykinin expression by dorsal root ganglion neurons in a rat model of neuropathic pain

Pain ◽  
1994 ◽  
Vol 58 (2) ◽  
pp. 219-231 ◽  
Author(s):  
James E. Marchand ◽  
Heinrich W. Wurm ◽  
Toshimasa Kato ◽  
Richard M. Kream
Keyword(s):  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Rat Model ◽  
Dorsal Root ◽  
Dorsal Root Ganglion Neurons ◽  
Ganglion Neurons

Contralateral Neuropathic Pain and Neuropathology in Dorsal Root Ganglion and Spinal Cord Following Hemilateral Nerve Injury in Rats

Spine ◽  
2008 ◽  
Vol 33 (12) ◽  
pp. 1344-1351 ◽  
Author(s):  
Satoshi Hatashita ◽  
Miho Sekiguchi ◽  
Hideo Kobayashi ◽  
Shin-ichi Konno ◽  
Shin-ichi Kikuchi
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Nerve Injury ◽  
Dorsal Root

scholarly journals Comparison of FDA-Approved Electrical Neuromodulation Techniques for Focal Neuropathic Pain: A Narrative Review of DRG, HF10, and Burst Neuromodulation

2021 ◽  
pp. E407-E423
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Spinal Cord Stimulation ◽  
High Frequency ◽  
Dorsal Root ◽  
Case Reports ◽  
Case Series ◽  
Dorsal Column ◽  
Small Sample

BACKGROUND: Evidence suggests that dorsal root ganglion stimulation (DRGS) is a more effective treatment for focal neuropathic pain (FNP) compared with tonic, paresthesia-based dorsal column spinal cord stimulation (SCS). However, new advancements in waveforms for dorsal column SCS have not been thoroughly studied or compared with DRGS for the treatment of FNP. OBJECTIVES: The purpose of this review was to examine the evidence for these novel technologies; to highlight the lack of high-quality evidence for the use of neuromodulation to treat FNP syndromes other than complex regional pain syndrome I or II of the lower extremity; to emphasize the absence of comparison studies between DRGS, burst SCS, and high-frequency SCS; and to underscore that consideration of all neuromodulation systems is more patient-centric than a one-size-fits-all approach. STUDY DESIGN: This is a review article summarizing case reports, case series, retrospective studies, prospective studies, and review articles. SETTING: The University of Miami, Florida. METHODS: A literature search was conducted from February to March 2020 using the PubMed and EMBASE databases and keywords related to DRGS, burst SCS, HF10 (high-frequency of 10 kHz), and FNP syndromes. All English-based literature from 2010 reporting clinical data in human patients were included. RESULTS: Data for the treatment of FNP using burst SCS and HF10 SCS are limited (n = 11 for burst SCS and n = 11 for HF10 SCS). The majority of these studies were small, single-center, nonrandomized, noncontrolled, retrospective case series and case reports with short follow-up duration. To date, there are only 2 randomized controlled trials for burst and HF10 for the treatment of FNP. LIMITATIONS: No studies were available comparing DRGS to HF10 or burst for the treatment of FNP. Data for the treatment of FNP using HF10 and burst stimulation were limited to a small sample size reported in mostly case reports and case series. CONCLUSIONS: FNP is a complex disease, and familiarity with all available systems allows the greatest chance of success. KEY WORDS: Dorsal root ganglion, high frequency, burst, spinal cord stimulation, neuromodulation, focal neuropathic pain

scholarly journals Intrathecal injection of bone marrow stromal cells attenuates neuropathic pain via inhibition of P2X4R in spinal cord microglia

2019 ◽  
Vol 16 (1) ◽  
Author(s):  
Yongbo Teng ◽  
Yang Zhang ◽  
Shouwei Yue ◽  
Huanwen Chen ◽  
Yujuan Qu ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Bone Marrow ◽  
Neuropathic Pain ◽  
Dorsal Root Ganglion ◽  
Dorsal Root ◽  
Purinergic Receptor ◽  
Intrathecal Injection ◽  
Transient Receptor Potential Vanilloid ◽  
Drg Neurons ◽  
Analgesic Effects

Abstract Background Neuropathic pain is one of the most debilitating of all chronic pain syndromes. Intrathecal (i.t.) bone marrow stromal cell (BMSC) injections have a favorable safety profile; however, results have been inconsistent, and complete understanding of how BMSCs affect neuropathic pain remains elusive. Methods We evaluated the analgesic effect of BMSCs on neuropathic pain in a chronic compression of the dorsal root ganglion (CCD) model. We analyzed the effect of BMSCs on microglia reactivity and expression of purinergic receptor P2X4 (P2X4R). Furthermore, we assessed the effect of BMSCs on the expression of transient receptor potential vanilloid 4 (TRPV4), a key molecule in the pathogenesis of neuropathic pain, in dorsal root ganglion (DRG) neurons. Results I.t. BMSC transiently but significantly ameliorated neuropathic pain behavior (37.6% reduction for 2 days). We found no evidence of BMSC infiltration into the spinal cord parenchyma or DRGs, and we also demonstrated that intrathecal injection of BMSC-lysates provides similar relief. These findings suggest that the analgesic effects of i.t. BMSC were largely due to the release of BMSC-derived factors into the intrathecal space. Mechanistically, we found that while i.t. BMSCs did not change TRPV4 expression in DRG neurons, there was a significant reduction of P2X4R expression in the spinal cord microglia. BMSC-lysate also reduced P2X4R expression in activated microglia in vitro. Coadministration of additional pharmacological interventions targeting P2X4R confirmed that modulation of P2X4R might be a key mechanism for the analgesic effects of i.t. BMSC. Conclusion Altogether, our results suggest that i.t. BMSC is an effective and safe treatment of neuropathic pain and provides novel evidence that BMSC’s analgesic effects are largely mediated by the release of BMSC-derived factors resulting in microglial P2X4R downregulation.

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