The Efficacy of Morphine, Pregabalin, Gabapentin, and Duloxetine on Mechanical Allodynia Is Different from That on Neuroma Pain in the Rat Neuropathic Pain Model

2012 ◽  
Vol 115 (1) ◽  
pp. 182-188 ◽  
Author(s):  
Rika Miyazaki ◽  
Tatsuo Yamamoto
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Allodynia ◽  
Pain Model ◽  
Neuropathic Pain Model

Rufinamide alleviates mechanical allodynia in a mouse neuropathic pain model

2011 ◽  
Vol 28 ◽  
pp. 193
Author(s):  
M. R. Suter ◽  
G. Kirschmann ◽  
H. Abriel ◽  
I. Decosterd
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Allodynia ◽  
Pain Model ◽  
Neuropathic Pain Model

Minocycline attenuates mechanical allodynia and expression of spinal NMDA receptor 1 subunit in rat neuropathic pain model

2012 ◽  
Vol 69 (3) ◽  
pp. 349-357 ◽  
Author(s):  
Shaofeng Pu ◽  
Yongming Xu ◽  
Dongping Du ◽  
Meirong Yang ◽  
Xin Zhang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nmda Receptor ◽  
Mechanical Allodynia ◽  
Pain Model ◽  
Neuropathic Pain Model

scholarly journals Mechanical Allodynia Assessment in a Murine Neuropathic Pain Model

BIO-PROTOCOL ◽  
2018 ◽  
Vol 8 (2) ◽  
Author(s):  
Serena Notartomaso ◽  
Pamela Scarselli ◽  
Paola Di Pietro ◽  
Giuseppe Battaglia ◽  
Amadeu Llebaria ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Allodynia ◽  
Pain Model ◽  
Neuropathic Pain Model

Attenuation of mechanical allodynia by clinically utilized drugs in a rat chemotherapy-induced neuropathic pain model

Pain ◽  
2004 ◽  
Vol 110 (1) ◽  
pp. 56-63 ◽  
Author(s):  
James J Lynch ◽  
Carrie L Wade ◽  
Chengmin M Zhong ◽  
Joseph P Mikusa ◽  
Prisca Honore
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Allodynia ◽  
Pain Model ◽  
Neuropathic Pain Model

Effects of site-directed GDNF overexpression on mechanical allodynia in a neuropathic pain model

2009 ◽  
Vol 65 ◽  
pp. S180
Author(s):  
Atsushi Sakai ◽  
Hideki Hanawa ◽  
Takashi Shimada ◽  
Hidenori Suzuki
Keyword(s):  
Neuropathic Pain ◽  
Mechanical Allodynia ◽  
Pain Model ◽  
Neuropathic Pain Model

Efficacy of the ketamine metabolite (2R,6R)-hydroxynorketamine in mice models of pain

2019 ◽  
Vol 44 (1) ◽  
pp. 111-117 ◽  
Author(s):  
Jeffrey S Kroin ◽  
Vaskar Das ◽  
Mario Moric ◽  
Asokumar Buvanendran
Keyword(s):  
Chronic Pain ◽  
Neuropathic Pain ◽  
Postoperative Pain ◽  
Mechanical Allodynia ◽  
Pain Syndrome ◽  
Saline Control ◽  
Pain Model ◽  
Time Period ◽  
Pain Models ◽  
Neuropathic Pain Model

Background and objectivesKetamine has been shown to reduce chronic pain; however, the adverse events associated with ketamine makes it challenging for use outside of the perioperative setting. The ketamine metabolite (2R,6R)-hydroxynorketamine ((2R,6R)-HNK) has a therapeutic effect in mice models of depression, with minimal side effects. The objective of this study is to determine if (2R,6R)-HNK has efficacy in both acute and chronic mouse pain models.MethodsMice were tested in three pain models: nerve-injury neuropathic pain, tibia fracture complex regional pain syndrome type-1 (CRPS1) pain, and plantar incision postoperative pain. Once mechanical allodynia had developed, systemic (2R,6R)-HNK or ketamine was administered as a bolus injection and compared with saline control in relieving allodynia.ResultsIn all three models, 10 mg/kg ketamine failed to produce sustained analgesia. In the neuropathic pain model, a single intraperitoneal injection of 10 mg/kg (2R,6R)-HNK elevated von Frey thresholds over a time period of 1–24hours compared with saline (F=121.6, p<0.0001), and three daily (2R,6R)-HNK injections elevated von Frey thresholds for 3 days compared with saline (F=33.4, p=0.0002). In the CRPS1 model, three (2R,6R)-HNK injections elevated von Frey thresholds for 3 days and then an additional 4 days compared with saline (F=116.1, p<0.0001). In the postoperative pain model, three (2R,6R)-HNK injections elevated von Frey thresholds for 3 days and then an additional 5 days compared with saline (F=60.6, p<0.0001).ConclusionsThis study demonstrates that (2R,6R)-HNK is superior to ketamine in reducing mechanical allodynia in acute and chronic pain models and suggests it may be a new non-opioid drug for future therapeutic studies.

scholarly journals Effect of Methylcobalamin on Voltage-Gated Sodium Channels (Vgscs ) Expression in Neuropathic Painanimal Model

2021 ◽  
Vol 14 (02) ◽  
pp. 1033-1038
Author(s):  
Endang Mutiawati ◽  
K.R.T. Lucas Meliala ◽  
Ginus Partadiredja ◽  
Dhirgo Adji ◽  
Raden Wasito
Keyword(s):  
Neuropathic Pain ◽  
Sodium Channels ◽  
Mechanical Allodynia ◽  
Spinal Nerve ◽  
Control Group ◽  
Pain Model ◽  
Voltage Gated ◽  
Voltage Gated Sodium Channels ◽  
Neuropathic Pain Model ◽  
First Onset

The objective of this study wasto assess the effect of methylcobalaminonmechanical allodynia and the voltage-gated sodium channels (VGSCs) expression of injured nerves in spinal nerve ligation-induced neuropathic pain model in animals.Three different doses of methylcobalamin were administrated intramuscularly into neuropathic pain rat model, twice a week for 14 weeks. The effect of methylcobalamin on neuropathic pain was assessed using mechanical allodynia (using the von Frey filaments) while its effect on VGSC expression was assessed using immunohistochemistry. ANOVA and independent t-test were employed to compared the effect of methylcobalamin on mechanical allodynia between groups.The size of von Frey filament that induced the first onset of mechanical allodynia was smaller in control group compared to 50µg methylcobalamin group (p=0.013) and methylcobalamin 100µg group (p=0.019). There is a dose–response relationship between methylcobalamin dose and the average duration of mechanical allodynia (43.8, 38.2, 30.6 and 29.6 days for control, 50µg, 100µg, and 150µg methylcobalamin group, respectively) with a significant different observed between control and 150µg methylcobalamin group only (p=0.027). Nerve tissues from all animals within control group expressed VGSC while all nerve tissues from both 100µg, and 150µg methylcobalamin, had no VGCS expression. In conclusion, methylcobalamin is potentially shorten the duration of mechanical allodynia and increase pain threshold in neuropathic pain animal model. These effects might associate with reduction of VGSC expression on the injured neurons.

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