Cellular sources of cyclooxygenase-1 and -2 up-regulation in the spinal dorsal horn after spinal nerve ligation

2014 ◽  
Vol 40 (4) ◽  
pp. 452-463 ◽  
Author(s):  
Yee Man Lau ◽  
Shing Chau Wong ◽  
Sin Wah Tsang ◽  
Wai Kit Lau ◽  
Ai Ping Lu ◽  
...  
2015 ◽  
Vol 56 (5) ◽  
pp. 1307 ◽  
Author(s):  
Hee Youn Hwang ◽  
Enji Zhang ◽  
Sangil Park ◽  
Woosuk Chung ◽  
Sunyeul Lee ◽  
...  

2013 ◽  
Vol 1519 ◽  
pp. 31-39 ◽  
Author(s):  
Enji Zhang ◽  
Min-Hee Yi ◽  
Youngkwon Ko ◽  
Hyun-Woo Kim ◽  
Je Hoon Seo ◽  
...  

2016 ◽  
Vol 41 (11) ◽  
pp. 2880-2889 ◽  
Author(s):  
Ryuji Terayama ◽  
Yuya Yamamoto ◽  
Noriko Kishimoto ◽  
Mitsuyasu Tabata ◽  
Kotaro Maruhama ◽  
...  

2014 ◽  
Vol 121 (2) ◽  
pp. 362-371 ◽  
Author(s):  
Masafumi Kimura ◽  
Hideaki Obata ◽  
Shigeru Saito

Abstract Background: Morphine produces powerful analgesic effects against acute pain, but it is not effective against neuropathic pain, and the mechanisms underlying this reduced efficacy remain unclear. Here, the authors compared the efficacy of systemic morphine between normal rats and rats with peripheral nerve injury, with a specific focus on descending serotonergic mechanisms. Methods: After L5 spinal nerve ligation injury, male Sprague–Dawley rats were subjected to behavioral testing, in vivo microdialysis of the spinal dorsal horn to determine serotonin (5-hydroxytryptamine [5-HT]) and noradrenaline release, and immunohistochemistry (n = 6 in each group). Results: Intraperitoneal administration of morphine (1, 3, or 10 mg/kg) produced analgesic effects in normal and spinal nerve ligation rats, but the effects were greater in normal rats (P < 0.001). Morphine increased 5-HT release (450 to 500% of the baseline), but not noradrenaline release, in the spinal dorsal horn via activation of serotonergic neurons in the rostral ventromedial medulla. Intrathecal pretreatment with ondansetron (3 μg), a 5-HT3 receptor antagonist, or 5,7-dihydroxytryptamine creatinine sulfate (100 μg), a selective neurotoxin for serotonergic terminals, attenuated the analgesic effect of morphine (10 mg/kg) in normal rats but increased the analgesic effect of morphine in spinal nerve ligation rats (both P < 0.05). Conclusions: Systemic administration of morphine increases 5-HT levels in the spinal cord, and the increase in 5-HT contributes to morphine-induced analgesia in the normal state but attenuates that in neuropathic pain through spinal 5-HT3 receptors. The plasticity of the descending serotonergic system may contribute to the reduced efficacy of systemic morphine in neuropathic pain.


2003 ◽  
Vol 98 (1) ◽  
pp. 203-208 ◽  
Author(s):  
Weiya Ma ◽  
Wei Du ◽  
James C. Eisenach

Background Systemic lidocaine and other local anesthetics reduce hypersensitivity states induced by both acute inflammation and peripheral nerve injury in animals and produce analgesia in some patients with chronic pain. The mechanisms underlying the antiallodynic effect of systemic lidocaine are unclear, although most focus is on peripheral mechanisms. Central mechanisms, particularly at the spinal dorsal horn level, are less known. In this study, the authors aimed to determine whether intrathecal lidocaine has an antiallodynic effect on established mechanical allodynia in two well-characterized neuropathic pain rat models: partial sciatic nerve ligation (PSNL) and spinal nerve ligation (SNL). Methods Lidocaine (100-300 micro g) was intrathecally injected in PSNL and SNL rats. The withdrawal threshold of both hind paws in response to mechanical stimulation was measured using a series of calibrated von Frey filaments. Results This single injection reduced ongoing tactile allodynia in PSNL and SNL rats. The antiallodynic effect of intrathecal lidocaine lasted longer in PSNL (> 3 days) than in SNL rats (< 3 days). Intraperitoneal lidocaine (300 micro g) had no effect on tactile allodynia in PSNL rats. In SNL rats, prior intrathecal lidocaine (200 and 300 micro g) potentiated the antiallodynic effect of intrathecal ketorolac, a nonselective cyclooxygenase inhibitor. Intrathecal ketorolac alone had no antiallodynic effect on SNL rats. However, prior intrathecal lidocaine (100 micro g) failed to potentiate the antiallodynic effect of intrathecal ketorolac. Conclusion The authors' data suggest that intrathecal lidocaine possibly suppressed the hyperexcitability of the dorsal horn neurons and likely interacted with eicosanoid systems in the spinal dorsal horn.


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