Peripheral Delta Opioid Receptors Mediate Formoterol Anti-allodynic Effect in a Mouse Model of Neuropathic Pain

Ceredig, Rhian Alice; Pierre, Florian; Doridot, Stéphane; Alduntzin, Unai; Hener, Pierre; Salvat, Éric; Yalçın, İpek; Gavériaux‐Ruff, Claire; Barrot, Michel; Massotte, Dominique

doi:10.3389/fnmol.2019.00324

Cited by 10 publications

(8 citation statements)

References 37 publications

(75 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…DORs are necessary to the antiallodynic action of chronic treatments with antidepressant drugs (Benbouzid et al, 2008a;Ceredig et al, 2018;Choucair Jaafar et al, 2014;Kremer et al, 2016;Kremer et al, 2018) and with β 2 adrenoceptor agonists (Ceredig et al, 2020;Choucair Jaafar et al, 2014;Kremer et al, 2020). In agreement with these findings, we found here that the action of a chronic treatment with the PDE4i rolipram on mechanical hypersensitivity also required DORs.…”

Section: Discussionsupporting

confidence: 90%

Antiallodynic action of phosphodiesterase inhibitors in a mouse model of peripheral nerve injury

et al. 2022

Self Cite

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 90%

Antiallodynic action of phosphodiesterase inhibitors in a mouse model of peripheral nerve injury

et al. 2022

Self Cite

View full text Add to dashboard Cite

“…These results suggest a mechanism similar to the one previously observed for antidepressant drugs, whose antiallodynic action has also been shown to be dependent upon DOP receptors. 9,16,19 In the Cuff model, it was also shown that sustained neuropathic pain condition was associated with a reduction of DOP receptor expression in small calcitonin gene-related peptide positive primary sensory neurons and in free nerve endings, that was not present in duloxetine 19 treated animals and that was partly corrected in formoterol 38 treated animals. In physiological conditions, DOP receptor agonists have little noticeable effect on nociception, as shown by pharmacological studies and data in DOP receptor deficient mice.…”

Section: Discussionmentioning

confidence: 99%

Delta opioid receptors are essential to the antiallodynic action of Β₂-mimetics in a model of neuropathic pain

et al. 2020

Self Cite

View full text Add to dashboard Cite

The adrenergic system, because of its reported implication in pain mechanisms, may be a potential target for chronic pain treatment. We previously demonstrated that b 2-adrenoceptors (b 2-ARs) are essential for neuropathic pain treatment by antidepressant drugs, and we showed that agonists of b 2-ARs, that is, b 2-mimetics, had an antiallodynic effect per se following chronic administration. To further explore the downstream mechanism of this action, we studied here the role of the opioid system. We used behavioral, genetic, and pharmacological approaches to test whether opioid receptors were necessary for the antiallodynic action of a short acting (terbutaline) and a long-acting (formoterol) b 2-mimetic. Using the Cuff model of neuropathic pain in mice, we showed that chronic treatments with terbutaline (intraperitoneal) or formoterol (orally) alleviated mechanical hypersensitivity. We observed that these b 2-mimetics remained fully effective in l-opioid and in j-opioid receptor deficient mice, but lost their antiallodynic action in d-opioid receptor deficient mice, either female or male. Accordingly, we showed that the d-opioid receptor antagonist naltrindole induced an acute relapse of allodynia in mice with neuropathic pain chronically treated with the b 2-mimetics. Such relapse was also observed following administration of the peripheral opioid receptor antagonist naloxone methiodide. These data demonstrate that the antiallodynic effect of longterm b 2-mimetics in a context of neuropathic pain requires the endogenous opioid system, and more specifically peripheral d-opioid receptors.

show abstract

“…This leads to the inhibition of Ca 2+ or Na + current, and subsequent inhibition of peripheral sensory neurons, which ultimately produces analgesia (Stein et al, 2003). In a variety of preclinical pain models such as inflammatory and neuropathic pain, the opioid receptors in the DRG are upregulated (Puehler et al, 2006;Ceredig et al, 2019). In addition, opioids produce more significant analgesic effects in injured tissues than in non-injured tissues (Stein et al, 2003;Vanderah et al, 2008).…”

Section: Discussionmentioning

confidence: 99%

Curcumin Exerts Antinociceptive Effects in Cancer-Induced Bone Pain via an Endogenous Opioid Mechanism

et al. 2021

View full text Add to dashboard Cite

Cancer pain is one of the main complications in advanced cancer patients, and its management is still challenging. Therefore, there is an urgent need to develop novel pharmacotherapy for cancer pain. Several natural products have attracted the interest of researchers. In previous studies, curcumin has proved to exhibit antitumor, antiviral, antioxidant, anti-inflammatory, and analgesic effects. However, the analgesic mechanism of curcumin has not been elucidated. Thus, in this study, we aimed to elucidate the antinociceptive potency and analgesic mechanism of curcumin in cancer-induced bone pain. Our results showed that consecutive curcumin treatment (30, 60, 120 mg/kg, i.p., twice daily for 11 days) produced significant analgesic activity, but had no effect on the progress of the bone cancer pain. Notably, pretreatment with naloxone, a non-selective opioid receptor antagonist, markedly reversed the antinociceptive effect induced by curcumin. Moreover, in primary cultured rat dorsal root ganglion (DRG) neurons, curcumin significantly up-regulated the expression of proopiomelanocortin (Pomc) and promoted the release of β-endorphin and enkephalin. Furthermore, pretreatment with the antiserum of β-endorphin or enkephalin markedly attenuated curcumin-induced analgesia in cancer-induced bone pain. Our present study, for the first time, showed that curcumin attenuates cancer-induced bone pain. The results also suggested that stimulation of expression of DRG neurons β-endorphin and enkephalin mediates the antinociceptive effect of curcumin in pain hypersensitivity conditions.

show abstract

Peripheral Delta Opioid Receptors Mediate Formoterol Anti-allodynic Effect in a Mouse Model of Neuropathic Pain

Cited by 10 publications

References 37 publications

Antiallodynic action of phosphodiesterase inhibitors in a mouse model of peripheral nerve injury

Antiallodynic action of phosphodiesterase inhibitors in a mouse model of peripheral nerve injury

Delta opioid receptors are essential to the antiallodynic action of Β₂-mimetics in a model of neuropathic pain

Curcumin Exerts Antinociceptive Effects in Cancer-Induced Bone Pain via an Endogenous Opioid Mechanism

Contact Info

Product

Resources

About

Peripheral Delta Opioid Receptors Mediate Formoterol Anti-allodynic Effect in a Mouse Model of Neuropathic Pain

Cited by 10 publications

References 37 publications

Antiallodynic action of phosphodiesterase inhibitors in a mouse model of peripheral nerve injury

Antiallodynic action of phosphodiesterase inhibitors in a mouse model of peripheral nerve injury

Delta opioid receptors are essential to the antiallodynic action of Β2-mimetics in a model of neuropathic pain

Curcumin Exerts Antinociceptive Effects in Cancer-Induced Bone Pain via an Endogenous Opioid Mechanism

Contact Info

Product

Resources

About

Delta opioid receptors are essential to the antiallodynic action of Β₂-mimetics in a model of neuropathic pain