scholarly journals Upregulation of Chemokine CXCL12 in the Dorsal Root Ganglia and Spinal Cord Contributes to the Development and Maintenance of Neuropathic Pain Following Spared Nerve Injury in Rats

2016 ◽  
Vol 32 (1) ◽  
pp. 27-40 ◽  
Author(s):  
Liying Bai ◽  
Xinru Wang ◽  
Zhisong Li ◽  
Cunlong Kong ◽  
Yonghui Zhao ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Nerve Injury ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Spared Nerve Injury ◽  
Chemokine Cxcl12

Neuronal expression of the ubiquitin ligase Nedd4-2 in rat dorsal root ganglia: Modulation in the spared nerve injury model of neuropathic pain

Neuroscience ◽  
2012 ◽  
Vol 227 ◽  
pp. 370-380 ◽  
Author(s):  
M. Cachemaille ◽  
C.J. Laedermann ◽  
M. Pertin ◽  
H. Abriel ◽  
R.-D. Gosselin ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
Dorsal Root Ganglia ◽  
Ubiquitin Ligase ◽  
Dorsal Root ◽  
Spared Nerve Injury ◽  
Injury Model ◽  
Neuronal Expression

scholarly journals Upregulation of Casein Kinase 1∊ in Dorsal Root Ganglia and Spinal Cord after Mouse Spinal Nerve Injury Contributes to Neuropathic Pain

2009 ◽  
Vol 5 ◽  
pp. 1744-8069-5-74 ◽  
Author(s):  
Eri Sakurai ◽  
Takashi Kurihara ◽  
Kasumi Kouchi ◽  
Hironao Saegusa ◽  
Shuqin Zong ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Neuropathic Pain ◽  
Nerve Injury ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Spinal Nerve ◽  
Casein Kinase ◽  
Casein Kinase 1

Changes in VGLUT1 and VGLUT2 expression in rat dorsal root ganglia and spinal cord following spared nerve injury

2016 ◽  
Vol 99 ◽  
pp. 9-15 ◽  
Author(s):  
Hong-Sheng Wang ◽  
Gang Yu ◽  
Zhi-Tong Wang ◽  
Shou-Pu Yi ◽  
Rui-Bin Su ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nerve Injury ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Spared Nerve Injury

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.

scholarly journals Elevated Expression of Fractalkine (CX3CL1) and Fractalkine Receptor (CX3CR1) in the Dorsal Root Ganglia and Spinal Cord in Experimental Autoimmune Encephalomyelitis: Implications in Multiple Sclerosis-Induced Neuropathic Pain

2013 ◽  
Vol 2013 ◽  
pp. 1-14 ◽  
Author(s):  
Wenjun Zhu ◽  
Crystal Acosta ◽  
Brian MacNeil ◽  
Claudia Cortes ◽  
Howard Intrater ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Spinal Cord ◽  
Neuropathic Pain ◽  
Experimental Autoimmune Encephalomyelitis ◽  
Protein Expression ◽  
Dorsal Root Ganglia ◽  
Dorsal Root ◽  
Autoimmune Encephalomyelitis ◽  
Receptor Cx3cr1 ◽  
Experimental Autoimmune

Multiple sclerosis (MS) is a central nervous system (CNS) disease resulting from a targeted autoimmune-mediated attack on myelin proteins in the CNS. The release of Th1 inflammatory mediators in the CNS activates macrophages, antibodies, and microglia resulting in myelin damage and the induction of neuropathic pain (NPP). Molecular signaling through fractalkine (CX3CL1), a nociceptive chemokine, via its receptor (CX3CR1) is thought to be associated with MS-induced NPP. An experimental autoimmune encephalomyelitis (EAE) model of MS was utilized to assess time dependent gene and protein expression changes of CX3CL1 and CX3CR1. Results revealed significant increases in mRNA and the protein expression of CX3CL1 and CX3CR1 in the dorsal root ganglia (DRG) and spinal cord (SC) 12 days after EAE induction compared to controls. This increased expression correlated with behavioural thermal sensory abnormalities consistent with NPP. Furthermore, this increased expression correlated with the peak neurological disability caused by EAE induction. This is the first study to identify CX3CL1 signaling through CX3CR1 via the DRG /SC anatomical connection that represents a critical pathway involved in NPP induction in an EAE model of MS.

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
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