Role of Asic3, Nav1.7 and Nav1.8 in Electroacupuncture-Induced Analgesia in a Mouse Model of Fibromyalgia Pain

2018 ◽  
Vol 36 (2) ◽  
pp. 110-116 ◽  
Author(s):  
Liang-Ta Yen ◽  
Yu-Chan Hsu ◽  
Jaung-Geng Lin ◽  
Ching-Liang Hsieh ◽  
Yi-Wen Lin

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.

2015 ◽  
Vol 523 (10) ◽  
pp. 1505-1528 ◽  
Author(s):  
Jie Su ◽  
Tianle Gao ◽  
Tiejun Shi ◽  
Qiong Xiang ◽  
Xiaojun Xu ◽  
...  

2013 ◽  
Vol 48 (6) ◽  
pp. 945-950 ◽  
Author(s):  
Mustafa Naziroğlu ◽  
Abdülhadi Cihangir Uğuz ◽  
Özgür Ismailoğlu ◽  
Bilal Çiğ ◽  
Cemil Özgül ◽  
...  

2020 ◽  
Vol 18 (10) ◽  
pp. 791-797
Author(s):  
Qiong Xiang ◽  
Jing-Jing Li ◽  
Chun-Yan Li ◽  
Rong-Bo Tian ◽  
Xian-Hui Li

Background: Our previous study has indicated that somatostatin potently inhibits neuropathic pain through the activation of its type 2 receptor (SSTR2) in mouse dorsal root ganglion and spinal cord. However, the underlying mechanism of this activation has not been elucidated clearly Objective: The aim of this study is to perform the pharmacological studies on the basis of sciatic nerve-pinch mice model and explore the underlying mechanism involving SSTR2. Methods: On the basis of a sciatic nerve-pinch injury model, we aimed at comparing the painful behavior and dorsal root ganglion neurons neurochemical changes after the SSTR2 antibody (anti- SSTR2;5μl,1μg/ml) administration in the mouse. Results: After pinch nerve injury, we found that the mechanical hyperalgesia and severely painful behavior (autotomy) were detected after the application of SSTR2 antibody (anti-SSTR2; 5μl, 1μg/ml) on the pinch-injured nerve. The up-regulated phosphorylated ERK (p-ERK) expression and the apoptotic marker (i.e., Bax) were significantly decreased in DRGs after anti-SSTR2 treatment. Conclusion: The current data suggested that inhibitory changes in proteins from the apoptotic pathway in anti-SSTR2-treated groups might be taking place to overcome the protein deficits caused by SSTR2 antibody and supported the new therapeutic intervention with SSTR2 antagonist for neuronal degeneration following nerve injury.


Author(s):  
Vishwanath Sankarasubramanian ◽  
Srinivas Chiravuri ◽  
Ehsan Mirzakhalili ◽  
Carlos J. Anaya ◽  
John Ryan Scott ◽  
...  

Author(s):  
Xiaohua Fan ◽  
Chuanwei Wang ◽  
Junting Han ◽  
Xinli Ding ◽  
Shaocan Tang ◽  
...  

2012 ◽  
Vol 71 (Suppl 1) ◽  
pp. A31.2-A32
Author(s):  
J Su ◽  
T J Shi ◽  
T L Gao ◽  
Z Wiesenfeld-Hallin ◽  
T Hökfelt ◽  
...  

2010 ◽  
Vol 152 (12) ◽  
pp. 2167-2172 ◽  
Author(s):  
Ayhan Kanat ◽  
Adem Yilmaz ◽  
Mehmet D. Aydin ◽  
Murat Musluman ◽  
Sare Altas ◽  
...  

Author(s):  
Jonathan M. Hagedorn ◽  
Brittney Misercola ◽  
Ashley Comer ◽  
Jeanmarie Tari-Blake ◽  
Chelsey M. Hoffmann ◽  
...  

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