Systemic synergism between codeine and morphine in three pain models in mice

Miranda, Hugo F.; Noriega, Viviana; Zepeda, Ramiro; Sierralta, Fernando; Prieto, Juan Carlos

doi:10.1016/s1734-1140(13)70966-6

Cited by 19 publications

(8 citation statements)

References 29 publications

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“…The observation that morphine reversed the acetic acidstimulated stretching in the present study is consistent with several reports (Meymandi and Sepehri, 2008;Miranda et al, 2008Miranda et al, , 2013. Acetic acid-stimulated stretching is associated with peripheral activation of peritoneal immune cells that release a cascade of proinflammatory factors, including the nociceptive cytokines tumor necrosis factor-α, interleukin-1 (IL-1) and IL-8 (Thomazzi et al, 1997;Ribeiro et al, 2000).…”

Section: Discussionsupporting

confidence: 93%

Distinct interactions of cannabidiol and morphine in three nociceptive behavioral models in mice

Neelakantan

Tallarida

Reichenbach

et al. 2015

Behavioural Pharmacology

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Cannabinoid and opioid agonists can display overlapping behavioral effects and the combination of these agonists is known to produce enhanced antinociception in several rodent models of acute and chronic pain. The present study investigated the antinociceptive effects of the nonpsychoactive cannabinoid, cannabidiol (CBD) and the µ-opioid agonist morphine, both alone and in combination, using three behavioral models in mice, to test the hypothesis that combinations of morphine and CBD would produce synergistic effects. The effects of morphine, CBD, and morphine/CBD combinations were assessed in the following assays: (a) acetic acid-stimulated stretching; (b) acetic acid-decreased operant responding for palatable food; and (c) hot plate thermal nociception. Morphine alone produced antinociceptive effects in all three models of acute nociception, whereas CBD alone produced antinociception only in the acetic acid-stimulated stretching assay. The nature of the interactions between morphine and CBD combinations were assessed quantitatively based on the principle of dose equivalence. Combinations of CBD and morphine produced synergistic effects in reversing acetic acid-stimulated stretching behavior, but subadditive effects in the hot plate thermal nociceptive assay and the acetic acid-decreased operant responding for palatable food assay. These results suggest that distinct mechanisms of action underlie the interactions between CBD and morphine in the three different behavioral assays and that the choice of appropriate combination therapies for the treatment of acute pain conditions may depend on the underlying pain type and stimulus modality.

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Section: Discussionsupporting

confidence: 93%

Distinct interactions of cannabidiol and morphine in three nociceptive behavioral models in mice

Neelakantan

Tallarida

Reichenbach

et al. 2015

Behavioural Pharmacology

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“…In this occasion, the tests used were tonic pain (acetic acid writhing test), phasic pain (tail flick test) and inflammatory pain (orofacial formalin test). Furthermore, results obtained are in agreement with previous reported different profiles of nociceptive activity of NSAIDs in algesiometer tests [7][8][9][10][11][12].…”

Section: Discussionsupporting

confidence: 92%

Non-steroidal Anti-inflammatory Drugs in Tonic, Phasic and Inflammatory Mouse Models

et al. 2019

Self Cite

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The principal mechanism of action of non-steroidal anti-inflammatory drugs (NSAIDs) is the inhibition of ciclooxigenases. In this study was evaluated if NSAIDs could induce antinociceptive differences according to the type of murine pain model. Male mice were injected intraperitoneally with meloxicam, diclofenac, piroxicam, metamizol, ibuprofen, naproxen and paracetamol in the writhing, tail flick and formalin orofacial tests and dose-response were analyzed to obtain the ED50 of each drugs. Administration of NSAIDs produced in a dose-dependent antinociception with different potency in the tests. The relative potency of NSAIDs among the tests shows a value of 5.53 in the orofacial formalin test in phase I and 6.34 in phase II between meloxicam and paracetamol; of 7.60 in the writhing test between meloxicam and paracetamol and of 8.46 in the tail flick test between ibuprofen and paracetamol. If the comparison is made for each NSAID in the different tests, the minimum value was 0.01 for between writhing and phase II of the orofacial formalin. Meanwhile, the highest power ratio was 11.71 for diclofenac between writhing and tail flick tests. In conclusion, the results suggests that intraperitoneal NSAIDs administration induce antinociceptive activity depending on the type of pain. The results support that NSAIDs administration, induce a wide variety of antinociceptive effect, depending on the type of pain. This suggest the participation of different mechanisms of action that can be added to the simple inhibition of COXs controlled by NSAIDs.

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“…The first phase is associated to direct stimulation of nociceptors, whereas the second phase reflects integration between nociceptors and spinal and brainstem signaling (Raboisson and Dallel 2004). Face rubbing with the ipsilateral forepaw due to formalin injection into the vibrissa pad has been mentioned as a specific nociceptive response in rats and mice (Donatti et al 2014;Reisi et al 2014;Miranda et al 2013;Tamaddonfard et al 2011;Luccarini et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Role of the thalamic submedius nucleus histamine H1 and H2 and opioid receptors in modulation of formalin-induced orofacial pain in rats

Erfanparast

Tamaddonfard

Taati

et al. 2015

Naunyn-Schmiedeberg's Arch Pharmacol

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Histamine and opioid systems are involved in supraspinal modulation of pain. In this study, we investigated the effects of separate and combined microinjections of agonists and antagonists of histamine H 1 and H 2 and opioid receptors into the thalamic submedius (Sm) nucleus on the formalin-induced orofacial pain. Two guide cannulas were implanted into the right and left sides of the Sm in ketamineand xylazine-anesthetized rats. Orofacial formalin pain was induced by subcutaneous injection of a diluted formalin solution (50 μl, 1.5 %) into the vibrissa pad. Face rubbing durations were recorded at 3-min blocks for 45 min. Formalin produced a biphasic pain response (first phase: 0-3 min and second phase: 15-33 min). Separate and combined microinjections of histamine H 1 and H 2 receptor agonists, 2-pyridylethylamine (2-PEA) and dimaprit, respectively, and opioid receptor agonist, morphine, attenuated the second phase of pain. The analgesic effects induced by 2-PEA, dimaprit, and morphine were blocked by prior microinjections of fexofenadine (a histamine H 1 receptor antagonist), famotidine (a histamine H 2 receptor antagonist), and naloxone (an opioid receptor antagonist), respectively. Naloxone also prevented 2-PEA-and dimaprit-induced antinociception, and the analgesic effect induced by morphine was inhibited by fexofenadine and famotidine. These results showed the involvement of histamine H 1 and H 2 and opioid receptors in the Sm modulation of orofacial pain. Opioid receptor might be involved in analgesia induced by activation of histamine H 1 and H 2 receptors and vice versa.

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Systemic synergism between codeine and morphine in three pain models in mice

Cited by 19 publications

References 29 publications

Distinct interactions of cannabidiol and morphine in three nociceptive behavioral models in mice

Distinct interactions of cannabidiol and morphine in three nociceptive behavioral models in mice

Non-steroidal Anti-inflammatory Drugs in Tonic, Phasic and Inflammatory Mouse Models

Role of the thalamic submedius nucleus histamine H1 and H2 and opioid receptors in modulation of formalin-induced orofacial pain in rats

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