scholarly journals Role of brainstem serotonin in analgesia produced by low-intensity exercise on neuropathic pain after sciatic nerve injury in mice

Pain ◽  
2015 ◽  
Vol 156 (12) ◽  
pp. 2595-2606 ◽  
Author(s):  
Franciane Bobinski ◽  
Tamara A.A. Ferreira ◽  
Marina M. Córdova ◽  
Patrícia A. Dombrowski ◽  
Cláudio da Cunha ◽  
...  
1999 ◽  
Vol 90 (5) ◽  
pp. 1382-1391 ◽  
Author(s):  
Tatsuo Yamamoto ◽  
Yoshihiko Sakashita

Background Cholecystokinin-B receptor activation has been reported to reduce morphine analgesia. Neuropathic pain is thought to be relatively refractory to opioids. One possible mechanisms for a reduced effect of morphine on neuropathic pain is the induction of cholecystokinin in the spinal cord by nerve injury. The authors evaluated the role of the spinal cholecystokinin-B receptor on morphine analgesia in two rat neuropathic pain models: chronic constriction injury and partial sciatic nerve injury. Methods A chronic constriction injury is created by placing four loosely tied ligatures around the right sciatic nerve. A partial sciatic nerve injury was created by tight ligation of one third to one half of the right sciatic nerve. All drugs were injected intrathecally 7 and 11 days after the nerve injury. The effect of the drugs was reflected in the degree of paw withdrawal latency to thermal nociceptive stimulation. The paw withdrawal latencies of injured and uninjured paws were measured 5, 15, 30, and 60 min after the drugs were injected. Results In the chronic constriction injury model, intrathecal morphine increased the paw withdrawal latencies of injured and uninjured paws. PD135158, a cholecystokinin-B receptor antagonist, potentiated the analgesic effect of morphine on injured and uninjured paws. In the partial sciatic nerve injury model, the effect of morphine on the injured paw was less potent than that on the uninjured paw, and PD135158 potentiated the morphine analgesia in the uninjured paw and had only a minor effect on the morphine analgesia in the injured paw. Conclusions The effectiveness of morphine for thermal hyperalgesia after nerve injury depends on the type of nerve injury. The role of the cholecystokinin-B receptor in morphine analgesia in thermal hyperalgesia after nerve injury also depends on the type of nerve injury.


2014 ◽  
Vol 564 ◽  
pp. 27-31 ◽  
Author(s):  
Masahiro Ohsawa ◽  
Junpei Mutoh ◽  
Shohei Yamamoto ◽  
Hiroaki Hisa

2019 ◽  
Vol 8 (02) ◽  
pp. 124-129
Author(s):  
Jia Yao ◽  
Zhu Yuzhen ◽  
High Xiao ◽  
Xuan Yang ◽  
Jianzhao Deng ◽  
...  

2020 ◽  
Author(s):  
Cheng-Fu wan ◽  
Bo-Han zhang ◽  
Dao-Song Dong ◽  
Tao Song

Abstract Background: Neuropathic pain (NP) can be treated effectively using pulsed radiofrequency (PRF). NP development and maintenance involves the essential neurotransmitter chemokine c-c motif ligand 2 (CCL2). The present study aimed to determine whether PRF regulated CCL2 expression in sciatic nerve injury (SNI) model rats.Methods: Sprague-Dawley rats were divided randomly into a sham group, an SNI group, and a PRF group. In the PRF group, L5 dorsal root ganglia received PRF treatment. After paw withdrawal mechanical threshold (PWMT) was examined, the expression levels of CCL2 and nuclear factor kappa B (NF-κB) in spinal dorsal horn were determined.Results: The PWMT in PRF group increased significantly compared with that of the SNI group (P < 0.05). The CCL2 and NF-κB expression levels in the PRF group were significant lower than those in the SNI group (P < 0.05).Conclusion: NP was effectively alleviated by PRF-mediated reductions in CCL2 expression via inhibition of NF-κB activation in the spinal cord of SNI model rats.


PAIN RESEARCH ◽  
1997 ◽  
Vol 12 (2) ◽  
pp. 131-137
Author(s):  
Takumi Nagaro ◽  
Kazushi Takaishi ◽  
Hitoshi Kojo ◽  
Elizabeth A Disbrow ◽  
John H Eisele

2015 ◽  
Vol 2015 ◽  
pp. 1-3 ◽  
Author(s):  
Halil Ekrem Akkurt ◽  
Haluk Gümüş ◽  
Hamit Göksu ◽  
Ömer Faruk Odabaşı ◽  
Halim Yılmaz

There are a restricted number of studies about usage of gabapentin for neuropathic pain treatment of pediatric patients. We shared a 12-year-old male case with severe neuropathic pain that hindered the rehabilitation programme for the loss of muscle power and movement limitation. Neuropathic pain developed after peripheral sciatic damage due to firearm traumatisation did not respond to other medical treatments but healed nearly completely after gabapentin usage.


2021 ◽  
Vol 99 ◽  
pp. 107918
Author(s):  
Hai-Ming Guo ◽  
Yu Zhang ◽  
Yan Zhang ◽  
Peng-Fei Jiao ◽  
Xiao-Chong Fan ◽  
...  

2018 ◽  
Vol 18 (4) ◽  
pp. 687-693 ◽  
Author(s):  
Tiansheng Shi ◽  
Jing-Xia Hao ◽  
Zsuzsanna Wiesenfeld-Hallin ◽  
Xiao-Jun Xu

Abstract Background and aims The clinical management of neuropathic pain remains a challenge. We examined the interaction between gabapentin and NMDA receptor antagonists dextromethrophan and MK-801 in alleviating neuropathic pain-like behaviors in rats after spinal cord or sciatic nerve injury. Methods Female and male rats were produced with Ischemic spinal cord injury and sciatic nerve injury. Gabapentin, dextromethorphan, MK-801 or drug combinations were injected with increasing doses. Mechanical response thresholds were tested with von Frey hairs to graded mechanical touch/pressure, and ethyl chloride spray was applied to assess the cold sensitivity before and after injuries. Results In spinally injured rats, gabapentin and dextromethorphan did not affect allodynia-like behaviors at doses of 30 and 20 mg/kg, respectively. In contrast, combination of 15 or 30 mg/kg gabapentin with dextromethorphan at 10 mg/kg produced total alleviation of allodynia to mechanical or cold stimulation. Further reducing the dose of gapapentin to 7.5 mg/kg and dextromethorphan to 5 mg/kg still produced significant effect. MK-801, another NMDA receptor antagonist, also enhanced the effect of gabapentin in spinally injured rats. Similar synergistic anti-allodynic effect between dextromethorphan and gabapentin was also observed in a rat model of partial sciatic nerve injury. No increased side effect was seen following the combination between gabapentin and dextromethorphan. Conclusions In conclusion, the present study suggested that combining NMDA receptor antagonists with gabapentin could provide synergistic effect to alleviate neuropathic pain and reduced side effects. Implications Combining NMDA receptor antagonists with gabapentin may provide a new approach in alleviating neuropathic pain with increased efficacy and reduced side effects.


2020 ◽  
Vol 21 (10) ◽  
pp. 3509 ◽  
Author(s):  
Alessio Filippo Peritore ◽  
Rosalba Siracusa ◽  
Roberta Fusco ◽  
Enrico Gugliandolo ◽  
Ramona D’Amico ◽  
...  

Inflammation is known to be an essential trigger of the pathological changes that have a critical impact on nerve repair and regeneration; moreover, damage to peripheral nerves can cause a loss of sensory function and produces persistent neuropathic pain. To date, various potential approaches for neuropathic pain have focused on controlling neuroinflammation. The aim of this study was to investigate the neuroprotective effects of a new association of ultramicronized Palmitoylethanolamide (PEAum), an Autacoid Local Injury Antagonist Amide (ALIAmide) with analgesic and anti-inflammatory properties, with Paracetamol, a common analgesic, in a rat model of sciatic nerve injury (SNI). The association of PEAum–Paracetamol, in a low dose (5 mg/kg + 30 mg/kg), was given by oral gavage daily for 14 days after SNI. PEAum–Paracetamol association was able to reduce hyperalgesia, mast cell activation, c-Fos and nerve growth factor (NGF) expression, neural histological damage, cytokine release, and apoptosis. Furthermore, the analgesic action of PEAum–Paracetamol could act in a synergistic manner through the inhibition of the NF-κB pathway, which leads to a decrease of cyclooxygenase 2-dependent prostaglandin E2 (COX-2/PGE2) release. In conclusion, we demonstrated that PEAum associated with Paracetamol was able to relieve pain and neuroinflammation after SNI in a synergistic manner, and this therapeutic approach could be relevant to decrease the demand of analgesic drugs.


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