μ opioid and CB1 cannabinoid receptor interactions: reciprocal inhibition of receptor signaling and neuritogenesis

Rios, Carl; Gomes, Ivone; Devi, Lakshmi A

doi:10.1038/sj.bjp.0706757

Cited by 328Cannabis and Cannabinoid ResearchReceptor Mechanisms and SignalingNeuropeptides and Animal Physiology

μ opioid and CB1 cannabinoid receptor interactions: reciprocal inhibition of receptor signaling and neuritogenesis

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Rios, Carl, Gomes, Ivone, Devi, Lakshmi A·2006·British Journal of Pharmacology

DOI 10.1038/sj.bjp.0706757PMC PMC1751792

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Abstract

Several studies have described functional interactions between opioid and cannabinoid receptors; the underlying mechanism(s) have not been well explored. One possible mechanism is direct receptor–receptor interactions, as has been demonstrated for a number of G‐protein‐coupled receptors. In order to investigate interactions between opioid and cannabinoid receptors, we epitope tagged μ, δ and κ opioid receptors with Renilla luciferase and CB1 cannabinoid or CCR5 chemokine receptors with yellow fluorescent protein and examined the extent of substrate hydrolysis induced bioluminescence resonance energy transfer (BRET) signal. We find that coexpression of opioid receptors with cannabinoid receptors, but not with chemokine receptors, leads to a significant increase in the level of BRET signal, suggesting that the opioid–cannabinoid interactions are receptor specific. In order to examine the implications of these interactions to signaling, we used GTP γ S binding and mitogen‐activated protein kinase (MAPK) phosphorylation assays and examined the effect of receptor activation on signaling. We find that the μ receptor‐mediated signaling is attenuated by the CB1 receptor agonist; this effect is reciprocal and is seen in heterologous cells and endogenous tissue expressing both receptors. In order to explore the physiological consequences of this interaction, we examined the effect of receptor activation on the extent of Src and STAT3 phosphorylation and neuritogenesis in Neuro‐2A cells. We find that the simultaneous activation of μ opioid and CB1 cannabinoid receptors leads to a significant attenuation of the response seen upon activation of individual receptors, implicating a role for receptor–receptor interactions in modulating neuritogenesis. British Journal of Pharmacology (2006) 148, 387–395. doi:10.1038/sj.bjp.0706757

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CB1 receptors and MORs share similar signal transduction pathways.
“Of importance, these receptors share similar signal transduction pathways (Rios et al, 2006).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Rios et al, 2006
CB1 receptors and MORs form heterodimers.
“In addition to the above described influence of the CB 1 receptor on neuronal dynorphin release, CB 1 receptors and MORs form heterodimers, which account for enhanced neuronal antinociceptive interactions of cannabinoids and opioids (Rios et al, 2006).”
From The endogenous cannabinoid system: a budding source of targets for treating inflammatory and neuropathic pain (2018) · cites this paper as Rios et al, 2006

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Self-citation

Authors: Rios, C., Gomes, I., & Devi, L. A.
Affiliations: Cornell University (US)
Icahn School of Medicine at Mount Sinai (US)
Corresponding author: Devi, Lakshmi A
ORCID: Gomes, Ivone
Devi, Lakshmi A
Venue: British Journal of Pharmacology
Publisher: Wiley
Published: 2006-06
Volume: 148
Issue: 4
Pages: 387-395
ISSN: 0007-1188 (ISSN-L)
1476-5381
DOI: 10.1038/sj.bjp.0706757
PMC: PMC1751792
OpenAlex: W1487872499
Cited by: 327
References: 42
Citations by year: 2026: 7 · 2025: 14 · 2024: 13 · 2023: 7 · 2022: 10 · 2021: 16 · 2020: 17 · 2019: 15 · 2018: 11 · 2017: 15 · 2016: 16 · 2015: 9 · 2014: 18 · 2013: 21 · 2012: 25
FWCI: 14.41
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor, 973 d)
Locations: British Journal of Pharmacology (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (DA08863)
National Institute on Drug Abuse (DA 08863, K05DA019521, R56DA008863, R37DA008863, DA19521, R01DA008863)
Topics: Health Sciences › Medicine › Pharmacology › Cannabis and Cannabinoid Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
Keywords: mu-opioid receptor, CB1 receptor, receptor-receptor interactions, opioid-cannabinoid interaction, neurite outgrowth, bioluminescence resonance energy transfer, CCR5 chemokine receptor, MAPK phosphorylation, Src phosphorylation, STAT3 phosphorylation, N2a cells
MeSH terms: Cells, Cultured, Humans, Phosphorylation, Signal Transduction, Guanosine 5'-O-(3-Thiotriphosphate), Neurites, Receptors, Opioid, mu, Enkephalin, Ala(2)-MePhe(4)-Gly(5)-, Receptor, Cannabinoid, CB1, Extracellular Signal-Regulated MAP Kinases

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μ opioid and CB1 cannabinoid receptor interactions: reciprocal inhibition of receptor signaling and neuritogenesis

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