Inhibition of Spinal Prostaglandin Synthesis Early after L5/L6 Nerve Ligation Prevents the Development of Prostaglandin-dependent and Prostaglandin-independent Allodynia in the Rat

Hefferan, Michael P.; O’Rielly, Darren D.; Loomis, Christopher W.

doi:10.1097/00000542-200311000-00027

Cited by 42 publications

(30 citation statements)

References 48 publications

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“…A host of other studies have demonstrated the efficacy of NSAIDS in a variety of NMDA sensitive pain models (Ghilardi et al, 2004;Matsunaga et al, 2007) (Hefferan et al, 2003;Ren and Dubner, 1993;Ren et al, 1992b;Zhao et al, 2000) (Malmberg and Yaksh, 1993a) (Dirig et al, 1998). Taken together, these data strongly imply that products of cyclooxygenase activation (prostanoids) are frequently downstream of NMDA receptor activation in vivo.…”

Section: Discussionmentioning

confidence: 99%

Secondary hyperalgesia in the rat first degree burn model is independent of spinal cyclooxygenase and nitric oxide synthase

Sorkin

Doom

Maruyama

et al. 2008

European Journal of Pharmacology

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Various animal models of pain are dependent on activation of different glutamate receptor subtypes. First-degree burn of the paw elicits a secondary hyperalgesia that is dependent on Ca 2++ permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), but not N-methyl-D-aspartate (NMDA) receptors. The present study takes advantage of that specificity by examining the effects of spinal pretreatments of agents on this secondary hyperalgesia. Rats with indwelling intrathecal catheters were pretreated with agents prior to paw injury. Mechanical withdrawal thresholds were measured before, and for three h after the injury.Spinal pretreatment with cyclooxygenase (10 and 30 μg (S)-(+)-ibuprofen; and 3 and 30 μg ketorolac) and nitric oxide synthase (33 and 100 μg N G Nitro-L-arginine methyl ester hydrochloride (L-NAME) and 10 μg thiocitrulline) inhibitors resulted in no specific anti-allodynia. In contrast, ziconotide (0.3, 1.0 and 3 μg), the N-type voltage gated calcium channel antagonist was very effective in blocking burn-induced sensitivity at all doses used. L-type (Diltiazam 230 μg) and P-type (Agatoxin IVA 0.3 μg) calcium channel blockers produced intermediate effects. Thus, cyclooxygenase and nitric oxide synthase are assumed not to be downstream of Ca 2++ permeable AMPA receptors. Voltage gated calcium channels blockers could exert their effects either pre-or post-synaptically.

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Section: Discussionmentioning

confidence: 99%

Secondary hyperalgesia in the rat first degree burn model is independent of spinal cyclooxygenase and nitric oxide synthase

Sorkin

Doom

Maruyama

et al. 2008

European Journal of Pharmacology

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“…Indeed, peripheral nerve injury induces an up-regulation of COX-1 and COX-2 in the spinal cord and peripheral nerves during the early phase of neuropathic pain development (Hefferan et al, 2003;Ma and Eisenach, 2002;Zhao et al, 2000). Furthermore, CCI in rats reduces glutamate transporter uptake activity in the spine, as well as increasing extracellular concentrations of arachidonic acid and glutamate (Sung et al, 2007).…”

Section: Discussionmentioning

confidence: 99%

Comparison of the antinociceptive effects of ibuprofen arginate and ibuprofen in rat models of inflammatory and neuropathic pain

et al. 2012

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“…Studies have shown the usefulness of acute or repetitive administration of indomethacin [Zhao et al, 2000;Takahashi et al, 2004] S-ibuprofen, SC-560 [Hefferan et al, 2003], naproxen [Padi and Kulkarni, 2004], and meloxicam [Takahashi et al, 2005] when drugs are given before or immediately after nerve injury. Accordingly, several studies have found that intrathecal injection of ketorolac, piroxicam, NS-398 [Lashbrook et al, 1999], indomethacin [Zhao et al, 2000], S-ketoprofen [Ossipov et al, 2000], rofecoxib [Padi and Kulkarni, 2004], and meloxicam [Takeda et al, 2005] does not reverse established neuropathic pain in rats.…”

Section: Antiallodynic Effect Of Metamizolmentioning

confidence: 99%

Synergistic antiallodynic interaction of the metamizol‐gabapentin combination

Ortega-Varela

Herrera

Caram-Salas

et al. 2009

Drug Development Research

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This study was designed to evaluate the possible antiallodynic interaction between metamizol and gabapentin in rats submitted to L5/L6 spinal nerve ligation. Metamizol, gabapentin, or a combination of both drugs were assessed after oral and intrathecal administration in neuropathic rats. Metamizol partially reduced tactile allodynia after intrathecal, but not oral, administration. Conversely, gabapentin reduced tactile allodynia in a dose-dependent manner after both administration routes. Oral administration of a constant dose of metamizol (600 mg/kg) significantly increased the gabapentininduced antiallodynic effect. Moreover, the gabapentin ED 50 value was lower in the presence than in the absence of metamizol. Intrathecal co-administration of metamizol and gabapentin in a dose-fixed ratio (0.5:0.5) reduced tactile allodynia in rats. The theoretical ED 30 value for the spinal combination estimated from the isobologram was 118.4712 mg, whereas that experimental ED 30 value was 66.2710.1 mg indicating a synergistic interaction. Results indicate that metamizol, a cyclo-oxygenase 2 inhibitor, is able to reduce tactile allodynia as well to increase the antiallodynic effect of gabapentin in the neuropathic rat. This combination could be useful to treat neuropathic pain in humans. Drug Dev

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Inhibition of Spinal Prostaglandin Synthesis Early after L5/L6 Nerve Ligation Prevents the Development of Prostaglandin-dependent and Prostaglandin-independent Allodynia in the Rat

Cited by 42 publications

References 48 publications

Secondary hyperalgesia in the rat first degree burn model is independent of spinal cyclooxygenase and nitric oxide synthase

Secondary hyperalgesia in the rat first degree burn model is independent of spinal cyclooxygenase and nitric oxide synthase

Comparison of the antinociceptive effects of ibuprofen arginate and ibuprofen in rat models of inflammatory and neuropathic pain

Synergistic antiallodynic interaction of the metamizol‐gabapentin combination

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