Anandamide decreases naloxone-precipitated withdrawal signs in mice chronically treated with morphine

Vela, Gema; Ruiz‐Gayo, Mariano; Fuentes, JoséA.

doi:10.1016/0028-3908(95)00032-2

Cited by 114 publications

(56 citation statements)

References 14 publications

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“…The suggested decrease in anandamide release may underlie the increased expression of striatal cannabinoid CB 1 receptors in opiate-dependent rodents described recently (Navarro et al, 2001), reflecting the induction of compensatory mechanisms such as upregulation of the cannabinoid CB 1 receptor. In agreement with this hypothesis, the administration of low doses of anandamide (5 mg/kg) attenuated naloxoneprecipitated opiate withdrawal (Vela et al, 1995).…”

supporting

confidence: 73%

“…Theoretically, these functional interactions might be useful for the development of therapeutic strategies for several neuropsychiatric disorders, including opiate addiction. This hypothesis was recently supported by results of studies with the endogenous cannabinoid, anandamide (Vela et al, 1995), or the selective cannabinoid CB 1 receptor antagonist, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboxamide, SR141716A (Ledent et al, 1999;Navarro et al, 2001), in animals models of opiate self-administration and dependence. These studies demonstrated that stimulation of cannabinoid CB 1 receptors attenuates opiate withdrawal, whereas cannabinoid CB 1 receptor blockade induces an opiate withdrawal syndrome in morphine-dependent rodents (Navarro et al, 1998;Vela et al, 1995).…”

mentioning

confidence: 82%

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Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404

Arco¹,

Navarro²,

Bilbao³

et al. 2002

European Journal of Pharmacology

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supporting

confidence: 73%

mentioning

confidence: 82%

Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404

Arco¹,

Navarro²,

Bilbao³

et al. 2002

European Journal of Pharmacology

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“…Anandamide acts on cannabinoid (CB) receptors, and also potentiates opioid action, as evidenced by its attenuation of naloxoneinduced morphine withdrawal in mice [15,16]. Hence, in patients receiving opioids like morphine, factors that increase anandamide levels, or decrease its hydrolysis would be expected to potentiate opioid effects, as would be expected with FAAH variants with reduced function affecting anandamide hydrolysis.…”

mentioning

confidence: 99%

Fatty Acid Amide Hydrolase–morphine Interaction Influences Ventilatory Response to Hypercapnia and Postoperative Opioid Outcomes in Children

et al. 2016

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Aim: Fatty acid amide hydrolase (FAAH) degrades anandamide, an endogenous cannabinoid. We hypothesized that FAAH variants will predict risk of morphine-related adverse outcomes due to opioid-endocannabinoid interactions. Patients & methods:In 101 postsurgical adolescents receiving morphine analgesia, we prospectively studied ventilatory response to 5% CO 2 (HCVR), respiratory depression (RD) and vomiting. Blood was collected for genotyping and morphine pharmacokinetics. Results: We found significant FAAH-morphine interaction for missense (rs324420) and several regulatory variants, with HCVR (p < 0.0001) and vomiting (p = 0.0339). HCVR was more depressed in patients who developed RD compared with those who did not (p = 0.0034), thus FAAH-HCVR association predicts risk of impending RD from morphine use. Conclusion: FAAH genotypes predict risk for morphine-related adverse outcomes.

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“…⌬ 9 -THC reduces naloxone-precipitated withdrawal in morphine-dependent rats and mice (Hine et al, 1975;Bhargava, 1976). The endogenous cannabinoid anandamide also decreases naloxone-precipitated morphine withdrawal (Vela et al, 1995). Furthermore, several studies indicate that the morphine withdrawal syndrome is markedly decreased in CB1-receptor knockout mice (Ledent et al, 1999;Lichtman et al, 2001).…”

mentioning

confidence: 99%

Modulation of Oral Morphine Antinociceptive Tolerance and Naloxone-Precipitated Withdrawal Signs by Oral Δ⁹-Tetrahydrocannabinol

Cichewicz

Welch²

2003

J Pharmacol Exp Ther

108

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Previous studies have demonstrated a functional interaction between cannabinoid and opioid systems in the development and expression of morphine tolerance and dependence. In these experiments, we examined the effect of a low oral dose of ⌬ 9 -tetrahydrocannabinol (⌬ 9 -THC) on the development of oral morphine tolerance and the expression of naloxone-precipitated morphine withdrawal signs of jumping and diarrhea in ICR mice. Chronic treatment with high-dose oral morphine produced a 3.12-fold antinociceptive tolerance. Tolerance to morphine was prevented in groups receiving a daily cotreatment with a nonanalgetic dose (20 mg/kg p.o.) of ⌬ 9 -THC, except when challenged with a very high dose of morphine. The chronic coadministration of low-dose ⌬ 9 -THC also reduced naloxone-precipitated (1 mg/kg s.c.) platform jumping by 50% but did not reduce diarrhea. In separate experiments, mice treated chronically with high-dose morphine p.o. were not cross-tolerant to ⌬ 9 -THC; in fact, these morphine-tolerant mice were more sensitive to the acute antinociceptive effects of ⌬ 9 -THC. ⌬ 9 -THC (20 mg/kg p.o.) also reduced naloxone-precipitated jumping but not diarrhea when administered acutely to morphine-tolerant mice. These results represent the first evidence that oral morphine tolerance and dependence can be circumvented by coadministration of a nonanalgetic dose of ⌬ 9 -THC p.o. In summary, cotreatment with a combination of morphine and ⌬ 9 -THC may prove clinically beneficial in that long-term morphine efficacy is maintained.The clinical use of morphine for long periods of time is limited by its propensity to cause tolerance and physical dependence after repeated administration. To overcome tolerance to the analgesic effects of morphine, higher doses are necessary for adequate pain relief but are often accompanied by undesirable side effects such as constipation, nausea, and respiratory depression (Ellison, 1993). Morphine tolerance has been developed in rodent models using subcutaneously implanted morphine pellets (Cicero and Meyer, 1973;Bhargava, 1978), but little is known about tolerance to oral doses of morphine in mice. Mao et al. (1996) observed a decrease in antinociception produced by oral morphine in rats as measured by the tail-flick test over a period of several days.Our laboratory and others have shown that combinations of cannabinoids with morphine profoundly enhance morphine-induced analgesia. ⌬ 9 -THC at a nonanalgetic dose administered p.o. to mice significantly enhances the potency of opioids such as morphine and codeine (Smith et al., 1998;Cichewicz et al., 1999). This enhancement is theorized to be due to a combination of morphine's direct effects on the -opioid receptor and the effect of endogenous opioids whose release is stimulated by ⌬ 9 -THC (Smith et al., 1994;Pugh et al., 1996). In addition, the CB1 cannabinoid receptor and -opioid receptor have been found to be colocalized in areas important for the expression of morphine abstinence: nucleus accumbens, septum, striatum, periaqueductal ...

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Anandamide decreases naloxone-precipitated withdrawal signs in mice chronically treated with morphine

Cited by 114 publications

References 14 publications

Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404

Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404

Fatty Acid Amide Hydrolase–morphine Interaction Influences Ventilatory Response to Hypercapnia and Postoperative Opioid Outcomes in Children

Modulation of Oral Morphine Antinociceptive Tolerance and Naloxone-Precipitated Withdrawal Signs by Oral Δ⁹-Tetrahydrocannabinol

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Anandamide decreases naloxone-precipitated withdrawal signs in mice chronically treated with morphine

Cited by 114 publications

References 14 publications

Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404

Attenuation of spontaneous opiate withdrawal in mice by the anandamide transport inhibitor AM404

Fatty Acid Amide Hydrolase–morphine Interaction Influences Ventilatory Response to Hypercapnia and Postoperative Opioid Outcomes in Children

Modulation of Oral Morphine Antinociceptive Tolerance and Naloxone-Precipitated Withdrawal Signs by Oral Δ9-Tetrahydrocannabinol

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Modulation of Oral Morphine Antinociceptive Tolerance and Naloxone-Precipitated Withdrawal Signs by Oral Δ⁹-Tetrahydrocannabinol