Central cyclooxygenase inhibitors reduced IL-1β-induced hyperalgesia in temporomandibular joint of freely moving rats

Ahn, Dong Kuk; Chae, Jang Seong; Choi, Hyo Sun; Kyung, Hee-Moon; Kwon, Oh Won; Park, Hyo‐Sang; Youn, Dong Ho; Bae, Yong Chul

doi:10.1016/j.pain.2005.06.009

Cited by 35 publications

(28 citation statements)

References 57 publications

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“…Data from other studies conducted either in vivo or ex-vivo suggests however that SC-560 effects are unrelated to COX-2 inhibition. For example bradykinin-mediated induction of nociceptor sensitization is inhibited by SC-560 but not NS-398 [22] and IL-1 induced hyperalgesia is prevented by NS-398 but not SC-560 [1]. In our study there was also a marked difference between the actions of SC-560 and NS-398 on the baseline responsiveness of meningeal nociceptors: local application of SC-560 did not reduce baseline mechanosensitivity while NS-398 had a marked inhibitory effect.…”

Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α induces sensitization of meningeal nociceptors mediated via local COX and p38 MAP kinase actions

Zhang

Kainz

Burstein

et al. 2011

Pain

127

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The proinflammatory cytokine TNF-alpha has been shown to promote activation and sensitization of primary afferent nociceptors. The downstream signaling processes that play a role in promoting this neuronal response remain however controversial. Increased TNF-alpha plasma levels during migraine attacks suggest that local interaction between this cytokine and intracranial meningeal nociceptors plays a role in promoting the headache. Here, using in vivo single unit recording in the trigeminal ganglia of anesthetized rats, we show that meningeal TNF-alpha action promotes a delayed mechanical sensitization of meningeal nociceptors. Using immunohistochemistry, we provide evidence for non-neuronal localization of the TNF receptors TNFR1 to dural endothelial vascular cells and TNFR2 to dural resident macrophages as well as to some CGRP-expressing dural nerve fibers. We also demonstrate that meningeal vascular TNFR1 is co-localized with COX-1 while the perivascular TNFR2 is co-expressed with COX-2. We further report here for the first time that TNF-alpha evoked sensitization of meningeal nociceptors is dependent upon local action of cyclooxygenase (COX). Finally, we show that local application of TNF-alpha to the meninges evokes activation of the p38 MAP kinase in dural blood vessels that also express TNFR1 and that pharmacological blockade of p38 activation inhibits TNF-alpha evoked sensitization of meningeal nociceptors. Our study suggests that meningeal action of TNF-alpha could play an important role in the genesis of intracranial throbbing headaches such as migraine through a mechanism that involves at least partly activation of non-neuronal TNFR1 and TNFR2 and downstream activation of meningeal non-neuronal COX and the p38 MAP kinase.

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Section: Discussionmentioning

confidence: 99%

Tumor necrosis factor-α induces sensitization of meningeal nociceptors mediated via local COX and p38 MAP kinase actions

Zhang

Kainz

Burstein

et al. 2011

Pain

127

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“…Although meal frequency remained depressed for 42 days, meal duration and not meal frequency correlated with the expression of IL-1β and CGRP. While cytokines and CGRP are important in continued TMJ nociception [53, 54] there are several possible explanations why meal duration normalized in the face of continued TMJ inflammation. The first possibility is that a certain threshold level of inflammation was necessary to evoke pain.…”

Section: Discussionmentioning

confidence: 99%

Measuring persistent temporomandibular joint nociception in rats and two mice strains

Kramer

Kerins

Schneiderman

et al. 2010

Physiology & Behavior

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Temporomandibular joint (TMJ) pain has been reported to last for prolonged periods in humans. In rodents a variety of methods have been used to measure TMJ nociception, but for most of these methods the period of measurement has been minutes to a couple of hours. In addition, most measurement protocols required restraint or training of the animal. Previous studies from our laboratory demonstrated that feeding behavior, particularly meal duration, was an indicator of TMJ nociception in unrestrained and untrained male and female Sprague Dawley rats for up to two days. In this study, we first found that injection of complete Freund's adjuvant (CFA) into the TMJ of rats significantly lengthened meal duration for 19 days and also decreased meal frequency for 42 days. Interestingly, the meal duration varied significantly from day to day within the 19 day period. TMJ interleukin-1β (IL-1β) and calcitonin gene-related peptide (CGRP) were significantly elevated in the TMJ tissues of CFA injected animals and the level of these markers was attenuated as the meal duration decreased with time. Control animals injected with saline into the TMJ or CFA into the knee did not show a significant lengthening in meal duration but did show a decrease in meal frequency. In a second study, DBA/1LacJ mice given TMJ CFA injections showed a significantly lengthened meal duration on four of the seven days measured using end-of-the meal definition of 5 or 10 minutes. No other meal pattern changed significantly. Two days post-CFA injection, the DBA/1LacJ mice showed significantly elevated interleukin-6 (IL-6), but not elevated IL-1β. Seven days post-injection, both IL-6 and IL-1β were significantly elevated. No change in CGRP was detected. In this study C57BL/6 mice also received TMJ CFA injections, but they did not show a lengthening in any meal pattern or significant increases in IL-1β, IL-6 or CGRP. Our data show, for the first time, that meal duration can be used to measure CFA-induced nociception in the TMJ over the course of several weeks in unrestrained rats and for up to seven days in the DBA/1LacJ mouse strain. In addition, C57BL/6 mice are resistant to CFA-induced TMJ nociception at the same dose used in the DBA/ 1LacJ mice.

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“…For an intracisternal injection, animals were anesthetized with pentobarbital sodium (40mg/kg, ip). Anesthetized rats were mounted on a stereotaxic frame and a polyethylene tube (PE10) was implanted for the intracisternal injection (Ahn et al, 2005, in press; Choi et al, 2003; Wang et al, 2002). The polyethylene tube was subcutaneously led to the top of the skull and secured by a stainless steel screw and dental acrylic resin on the skull.…”

Section: Methodsmentioning

confidence: 99%

Intramuscular administration of morphine reduces mustard oil‐induced craniofacial muscle pain behavior in lightly anesthetized rats

Han

Lee

Lim

et al. 2008

European Journal of Pain

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The present study investigated the role of peripheral opioid receptors in mustard oil-induced nociceptive behavior and inflammation in the masseter muscles of lightly anesthetized rats. Experiments were carried out on male Sprague-Dawley rats weighing between 300 and 400 g. After initial anesthesia with sodium pentobarbital (40 mg/kg, i.p.), one femoral vein was cannulated and connected to an infusion pump for the intravenous infusion of sodium pentobarbital. The rate of infusion was adjusted to provide a constant level of anesthesia. Mustard oil (MO, 30 microl) was injected into the mid-region of the left masseter muscle via a 30-gauge needle. Intramuscularly-administered morphine significantly reduced shaking behavior but not MO-induced inflammation. Intramuscular pretreatment with naloxone, an opioid receptor antagonist, reversed antinociception produced by intramuscularly-administered morphine, while intracisternal administration of naloxone did not affect the antinociception of peripheral morphine. Pretreatment with d-Pen-Cys-Tyr-D-Trp-Orn-Thr-Pen-Thr-NH2 (CTOP), a mu opioid receptor antagonist, but not naltrindole, a delta opioid receptor antagonist, nor norbinaltorphimine (nor-BNI), a kappa opioid receptor antagonist, reversed intramuscularly-administered morphine-induced antinociception. These results indicate that intramuscularly-administered morphine produces antinociception in craniofacial muscle nociception and that this intramuscularly-administered morphine-induced antinociception is mediated by a peripheral mu opioid receptor. Our observations further support the clinical approach of administering opioids in the periphery for the treatment of craniofacial muscle nociception.

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Central cyclooxygenase inhibitors reduced IL-1β-induced hyperalgesia in temporomandibular joint of freely moving rats

Cited by 35 publications

References 57 publications

Tumor necrosis factor-α induces sensitization of meningeal nociceptors mediated via local COX and p38 MAP kinase actions

Tumor necrosis factor-α induces sensitization of meningeal nociceptors mediated via local COX and p38 MAP kinase actions

Measuring persistent temporomandibular joint nociception in rats and two mice strains

Intramuscular administration of morphine reduces mustard oil‐induced craniofacial muscle pain behavior in lightly anesthetized rats

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