Allodynia evoked by intrathecal administration of prostaglandin E2 to conscious mice

Minami, Toshiaki; Uda, Rumiko; Horiguchi, S; Ito, Seiji; Hyodo, Masayoshi; Hayaishi, Osamu

doi:10.1016/0304-3959(94)90226-7

Cited by 129 publications

(71 citation statements)

References 35 publications

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“…Taken together, our findings suggest that prostaglandin released in the DRG activates an autocrine signaling mechanism in primary afferent neurons to sensitize them. Indeed, prostanoid receptors are present either in the spinal cord or in the DRG (29) and intrathecal administration of the EP receptor agonists induced hyperalgesia (30). However, it is important to point out that the total volume of injection of COXinhibitors or EP antagonists into the L5-DRG was 2 μL.…”

Section: Discussionmentioning

confidence: 99%

“…6). Because inflammatory hyperalgesia involves PKCe translocation to the membrane of primary afferent neurons (16,17), this (30,70, 100, or 300 μg) administered into the L5-DRG prevented the hyperalgesia induced by IL-1β (0.5 pg per paw) in the L5 peripheral field. Indomethacin, valeryl salicylate, SC-236, or their vehicles were administered 30 min before IL-1β and the hyperalgesia was evaluated 3 h after its administration.…”

Section: Inflammatory Hyperalgesia In Peripheral Tissue Induces Pkcementioning

confidence: 95%

See 1 more Smart Citation

Peripheral inflammatory hyperalgesia depends on the COX increase in the dorsal root ganglion

Araldi

Ferrari

Lotufo

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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It is well established that dorsal root ganglion (DRG) cells synthesize prostaglandin. However, the role that prostaglandin plays in the inflammatory hyperalgesia of peripheral tissue has not been established. Recently, we have successfully established a technique to inject drugs (3 μL) directly into the L5-DRG of rats, allowing in vivo identification of the role that DRG cell-derived COX-1 and COX-2 play in the development of inflammatory hyperalgesia of peripheral tissue. IL-1β (0.5 pg) or carrageenan (100 ng) was administered in the L5-peripheral field of rat hindpaw and mechanical hyperalgesia was evaluated after 3 h. Administration of a nonselective COX inhibitor (indomethacin), selective COX-1 (valeryl salicylate), or selective COX-2 (SC-236) inhibitors into the L5-DRG prevented the hyperalgesia induced by IL-1β. Similarly, oligodeoxynucleotide-antisense against COX-1 or COX-2, but not oligodeoxynucleotide-mismatch, decreased their respective expressions in the L5-DRG and prevented the hyperalgesia induced by IL-1β in the hindpaw. Immunofluorescence analysis demonstrated that the amount of COX-1 and COX-2, constitutively expressed in TRPV-1 + cells of the DRG, significantly increased after carrageenan or IL-1β administration. In addition, indomethacin administered into the L5-DRG prevented the increase of PKCe expression in DRG membrane cells induced by carrageenan. Finally, the administration of EP1/EP2 (7.5 ng) or EP4 (10 μg) receptor antagonists into L5-DRG prevented the hyperalgesia induced by IL-1β in the hindpaw. In conclusion, the results of this study suggest that the inflammatory hyperalgesia in peripheral tissue depends on activation of COX-1 and COX-2 in C-fibers, which contribute to the induction and maintenance of sensitization of primary sensory neurons.D uring tissue injury, prostaglandin-E 2 (PGE 2 ) is produced by the activation of the enzyme cyclooxygenase (COX) to play an important role in inflammatory hyperalgesia. PGE 2 sensitizes peripheral nociceptors through the activation of PGE 2 receptors (EP) (1). This sensitization, characterized by a reduction of nociceptive threshold and by an increase in peripheral afferent neuron responsiveness, is the main feature of inflammatory hyperalgesia in the peripheral tissue. The widespread use of nonsteroidal antiinflammatory drugs to control inflammatory hyperalgesia exemplifies the relevance of PGE 2 for the development of inflammatory hyperalgesia. These drugs decrease peripheral inflammatory hyperalgesia by inhibiting COX and, therefore, by preventing the synthesis of PGE 2 (2, 3).The COX enzyme is expressed in two major isoforms, COX-1 and COX-2, with different biological functions (4), although both play a role in the inflammatory hyperalgesia (5, 6). The isoform of COX constitutively expressed in dorsal root ganglion (DRG) is still unclear. Although COX-1 mRNA and, to a lesser extent, COX-2 mRNA have been detected in DRG cultures (7) under basal conditions, immunohistochemical studies have shown that DRG cells express only COX-1, but not C...

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Section: Discussionmentioning

confidence: 99%

Section: Inflammatory Hyperalgesia In Peripheral Tissue Induces Pkcementioning

confidence: 95%

Peripheral inflammatory hyperalgesia depends on the COX increase in the dorsal root ganglion

Araldi

Ferrari

Lotufo

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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“…The synergistic action of N/OFQ and NST is really surprising; because studies reported on their opposite effects in several biological functions [3][4][5][6][7][8]22,23]. However these studies were carried out in the Central Nervous System (CNS) and gave no information about the peripheral interaction of these two neuropeptides.…”

Section: Amentioning

confidence: 99%

“…NST was thought to be a functional antagonist of N/OFQ on the basis of their effects in the central nervous system [3][4][5][6][7][8]. Although N/OFQ has no affinity to opiate receptors; interaction was reported between the N/OFQ and dynorphin in neuropathic pain [9].…”

Section: Introductionmentioning

confidence: 99%

Uterus-Relaxing Effects of Nociceptin and Nocistatin: Studies on Preterm and Term-Pregnant Human Myometrium In vitro

BH¹

2013

Reprod Sys Sexual Disorders

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The endogenous neuropeptides nociceptin/orphanin FQ and nocistatin translated from the prepronociceptin gene exert a relaxant effect on the rat uterus. Previous studies have reported their role in pain transmission in the central nervous system both in rodents and in humans, but to date only limited information is available on their effects in the periphery, and there are no data on their presence in the human uterus.The expression of prepronociceptin mRNA in the human uterus was confirmed by an RT-PCR technique. In vitro contractility studies of the action of nociceptin and nocistatin on human uterine tissues were performed in an isolated organ system. Human myometrial strips from cesarean sections at full-term pregnancy and at preterm labor were stimulated with oxytocin, and the relaxant effects of nociceptin and nocistatin were studied.The level of prepronociceptin mRNA was significantly decreased in full-term pregnant uterus samples as compared with preterm pregnancy samples. Nociceptin and nocistatin significantly and dose-dependently inhibited the oxytocinevoked contractions in the human uterus. In the presence of nocistatin, the uterus-relaxant effect of nociceptin was enhanced. In contrast, nociceptin did not alter the uterus-relaxant effect of nocistatin.We conclude that locally generated nociceptin and nocistatin both exert a relaxant effect on the human uterus, and nocistatin can potentiate the relaxant effect of nociceptin, though for this to occur nocistatin administration must precede the administration of nociceptin.

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“…A radiant heat source was then focused onto the plantar surface of a hind paw. The test involved placing a mouse on a hot plate maintained at 55 ºC and recording the time to first response (foot licking, jumping, or rapidly removing paws), as described by Minami et al [14] . A timer stopped automatically when withdrawal of the paw was detected by a photodetector (a cut-off value of 30 s was used to prevent tissue damage).…”

Section: Hot-plate Testmentioning

confidence: 99%

Intracisternal or intrathecal glycine, taurine, or muscimol inhibit bicuculline-induced allodynia and thermal hyperalgesia in mice

Lim

2010

Acta Pharmacol Sin

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Aim: To investigate the effects of GABA and glycine on analgesia in the central nervous system. Methods: Glycine, taurine, or muscimol was injected with bicuculline into the cistern magna or the lumbar subarachnoidal space in ICR mice. The effects on bicuculline-induced allodynia in a touch-evoked agitation test and on pain threshold index in a hot-plate test were assessed. Results: The dosages of the amino acids administered with bicuculline had no effect on motor behavior in conscious mice. Glycine or muscimol reduced bicuculline-induced allodynia regardless of the administration site, whereas intrathecal taurine reduced bicucullineinduced allodynia. Glycine, taurine, and muscimol all antagonized the effects induced by bicuculline in the hot-plate test, regardless of the administration site. Conclusion: Glycine, taurine, and muscimol were found to have anti-allodynic and anti-thermal hyperalgesic properties in vivo. These observations suggest an interaction between glycine and GABA receptors during the regulation of antinociception.

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Allodynia evoked by intrathecal administration of prostaglandin E2 to conscious mice

Cited by 129 publications

References 35 publications

Peripheral inflammatory hyperalgesia depends on the COX increase in the dorsal root ganglion

Peripheral inflammatory hyperalgesia depends on the COX increase in the dorsal root ganglion

Uterus-Relaxing Effects of Nociceptin and Nocistatin: Studies on Preterm and Term-Pregnant Human Myometrium In vitro

Intracisternal or intrathecal glycine, taurine, or muscimol inhibit bicuculline-induced allodynia and thermal hyperalgesia in mice

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