Attenuation of morphine-induced dependence and tolerance by ceftriaxone and amitriptyline in mice

Habibiasl, B; Vaez, Haleh; Najafi, Moslem; Bidaghi, Ali; Ghanbarzadeh, Saeed

doi:10.1016/j.aat.2014.11.001

Cited by 21 publications

(15 citation statements)

References 51 publications

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“…The analgesic effects of NSAIDs like diclofenac, paracetamol, aspirin, and metamizol, can be abolished by the opioid receptor antagonist, NLX [Vanegas et al, ]. It has also has been reported that CXF, but not CLAV, attenuates the development of tolerance to the antinociceptive effect of morphine and reduces NLX‐precipitated withdrawal [Habibi‐Asl et al, ; Hajhashemi and Dehdashti, ]. In both cases, the effects evaluated may be related to release of endogenous opioids.…”

Section: Discussionmentioning

confidence: 99%

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Ochoa-Aguilar

Sotomayor-Sobrino

Jaimez

et al. 2017

Drug Development Research

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Preclinical Research The aim of this study was to determine the antiallodynic effect of acute administration of the β-lactam antimicrobials, ceftriaxone (CFX) and clavulanic acid (CLAV), for the control of established pain on a model of neuropathic pain (NP). We also investigated the involvement of dopaminergic and opioidergic pathways as well as alterations in serum concentrations of TNF-α in the antiallodynic actions of these drugs. CFX, CLAV, or gabapentin (GAP), a reference drug, were administered i.p. twelve days after constriction of the sciatic nerve in rats. Mechanic and cold allodynia were evaluated for 3 h and alterations in serum concentration of TNF-α determined. Both CFX and CLAV had antiallodynic effects in response to mechanical and cold stimulation, similar to GAP. The antiallodynic effects of CFX and CLAV were blocked by haloperidol (HAL), a D2 receptor antagonist, and by naloxone (NLX), an opioid receptor antagonist. Additionally, serum TNF-α levels were attenuated following CFX and CLAV administration. These results suggest that acute administration of CFX and CLAV may represent a promising approach for treating the acute allodynia of NP, and that the mechanisms involved in these effects involve activation of dopaminergic and opioidergic pathways as well as modulation of TNF-α production. Drug Dev Res 78 : 105-115, 2017. © 2017 Wiley Periodicals, Inc.

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Section: Discussionmentioning

confidence: 99%

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Ochoa-Aguilar

Sotomayor-Sobrino

Jaimez

et al. 2017

Drug Development Research

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“…Morphine suppresses many types of pain, but tolerance, physical dependence, and unwanted side effects limit its clinical use (Trang et al, 2007). Identification of therapeutic strategies for blocking opioid tolerance and dependence has therefore evolved as an area of intense research interest (Habibi-Asl et al, 2014;Mansouri, et al, 2015;Hassanipour et al, 2016;Hosseinzadeh et al, 2016). Adjunctive pharmacotherapies that combine mechanistically distinct analgesics represent one such approach.…”

Section: Introductionmentioning

confidence: 99%

Slowly Signaling G Protein–Biased CB₂Cannabinoid Receptor Agonist LY2828360 Suppresses Neuropathic Pain with Sustained Efficacy and Attenuates Morphine Tolerance and Dependence

et al. 2017

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The CB cannabinoid agonist LY2828360 lacked both toxicity and efficacy in a clinical trial for osteoarthritis. Whether LY2828360 suppresses neuropathic pain has not been reported, and its signaling profile is unknown. In vitro, LY2828360 was a slowly acting but efficacious G protein-biased CB agonist, inhibiting cAMP accumulation and activating extracellular signal-regulated kinase 1/2 signaling while failing to recruit arrestin, activate inositol phosphate signaling, or internalize CB2 receptors. In wild-type (WT) mice, LY2828360 (3 mg/kg per day i.p. × 12 days) suppressed chemotherapy-induced neuropathic pain produced by paclitaxel without producing tolerance. Antiallodynic efficacy of LY2828360 was absent in CB knockout (KO) mice. Morphine (10 mg/kg per day i.p. × 12 days) tolerance developed in CBKO mice but not in WT mice with a history of LY2828360 treatment (3 mg/kg per day i.p. × 12 days). LY2828360-induced antiallodynic efficacy was preserved in WT mice previously rendered tolerant to morphine (10 mg/kg per day i.p. × 12 days), but it was absent in morphine-tolerant CBKO mice. Coadministration of LY2828360 (0.1 mg/kg per day i.p. × 12 days) with morphine (10 mg/kg per day × 12 days) blocked morphine tolerance in WT but not in CBKO mice. WT mice that received LY2828360 coadministered with morphine exhibited a trend ( = 0.055) toward fewer naloxone-precipitated jumps compared with CBKO mice. In conclusion, LY2828360 is a slowly signaling, G protein-biased CB agonist that attenuates chemotherapy-induced neuropathic pain without producing tolerance and may prolong effective opioid analgesia while reducing opioid dependence. LY2828360 may be useful as a first-line treatment in chemotherapy-induced neuropathic pain and may be highly efficacious in neuropathic pain states that are refractive to opioid analgesics.

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“…This method was performed, according to Habib-Asl [ 26 ]. Mice were divided into four groups ( n = 7 per group) as follows: (1) daily injection of saline, (2) daily injection of morphine (50 mg/kg, i.p.…”

Section: Methodsmentioning

confidence: 99%

Two New βN-Alkanoyl-5-Hydroxytryptamides with Relevant Antinociceptive Activity

et al. 2021

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In this work, we describe a new route for the synthesis and the antinociceptive effects of two new βN-alkanoyl-5-hydroxytryptamides (named C20:0-5HT and C22:0-5HT). The antinociceptive activities were evaluated using well-known models of thermal-induced (reaction to a heated plate, the hot plate model) or chemical-induced (licking response to paw injection of formalin, capsaicin, or glutamate) nociception. The mechanism of action for C20:0-5HT and C22:0-5HT was evaluated using naloxone (opioid receptor antagonist, 1 mg/kg), atropine (muscarinic receptor antagonist, 1 mg/kg), AM251 (cannabinoid CB1 receptor antagonist, 1 mg/kg), or ondansetron (5-HT3 serotoninergic receptor antagonist, 0.5 mg/kg) 30 min prior to C20:0-5HT or C22:0-5HT. The substances both presented significant effects by reducing licking behavior induced by formalin, capsaicin, and glutamate and increasing the latency time in the hot plate model. Opioidergic, muscarinic, cannabinoid, and serotoninergic pathways seem to be involved in the antinociceptive activity since their antagonists reversed the observed effect. Opioid receptors are partially involved due to tolerant mice demonstrating less antinociception when treated with both compounds. Our data showed a quicker and simpler route for the synthesis of the new βN-alkanoyl-5-hydroxytryptamides. Both compounds demonstrated significant antinociceptive effects. These new compounds could be used as a scaffold for the synthesis of analogues with promising antinociceptive effects.

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Attenuation of morphine-induced dependence and tolerance by ceftriaxone and amitriptyline in mice

Abstract: Results indicate that the treatment with ceftriaxone and amitriptyline, alone or in combination, could attenuate the development of morphine-induced tolerance and dependence.

Cited by 21 publications

References 51 publications

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Slowly Signaling G Protein–Biased CB₂Cannabinoid Receptor Agonist LY2828360 Suppresses Neuropathic Pain with Sustained Efficacy and Attenuates Morphine Tolerance and Dependence

Two New βN-Alkanoyl-5-Hydroxytryptamides with Relevant Antinociceptive Activity

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Attenuation of morphine-induced dependence and tolerance by ceftriaxone and amitriptyline in mice

Abstract: Results indicate that the treatment with ceftriaxone and amitriptyline, alone or in combination, could attenuate the development of morphine-induced tolerance and dependence.

Cited by 21 publications

References 51 publications

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Antiallodynic Activity of Ceftriaxone and Clavulanic Acid in Acute Administration is Associated with Serum TNF‐α Modulation and Activation of Dopaminergic and Opioidergic Systems

Slowly Signaling G Protein–Biased CB2Cannabinoid Receptor Agonist LY2828360 Suppresses Neuropathic Pain with Sustained Efficacy and Attenuates Morphine Tolerance and Dependence

Two New βN-Alkanoyl-5-Hydroxytryptamides with Relevant Antinociceptive Activity

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Slowly Signaling G Protein–Biased CB₂Cannabinoid Receptor Agonist LY2828360 Suppresses Neuropathic Pain with Sustained Efficacy and Attenuates Morphine Tolerance and Dependence