ArticlePsychopharmacology2021
Cannabinoid receptor GPR55 activation blocks nicotine use disorder by regulation of AMPAR phosphorylation.
Article in Psychopharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Nicotine replacement therapy: insights into the mechanisms and potential of nicotine receptor pathway.American journal of translational research · 2025Review
- Modulation of neuroinflammation and oxidative stress by targeting GPR55 - new approaches in the treatment of psychiatric disorders.Molecular psychiatry · 2024Review
- Article
- Cannabidiol as a potential cessation therapeutic: Effects on intravenous nicotine self-administration and withdrawal symptoms in mice.Neuropharmacology · 2024Article
- GPR55 is expressed in glutamate neurons and functionally modulates drug taking and seeking in rats and mice.Translational psychiatry · 2024Article
- New Insights in the Involvement of the Endocannabinoid System and Natural Cannabinoids in Nicotine Dependence.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
rationaleNicotine use disorder can alter synaptic plasticity correlated with learning and memory process. G protein-coupled receptor 55 (GPR55), a novel cannabinoid receptor, which is highly expressed in the central nervous system, plays a prominent role in learning and memory. However, the role of GPR55 in nicotine use disorder remains unclear.
methodsIn this study, we used the conditioned place preference (CPP) paradigm, a standard and well-established model for evaluating the rewarding effect of drug abuse, to investigate nicotine use disorder behavior in mice. After behavioral tests, the effect of GPR55 on nicotine response was evaluated using Western blotting, immunofluorescence staining, whole-cell patch-clamp recordings, and ELISA.
resultsGPR55 activation significantly reduced nicotine-CPP behavior by decreasing the spontaneous excitatory postsynaptic currents frequency in the nucleus accumbens (NAc) and the release of dopamine in serum. Furthermore, we found that the inhibition effects of nicotine response were mediated by phosphorylation of AMPAR. The PI3K-Akt signaling was involved in nicotine-CPP via GPR55 activation.
conclusionOur findings showed that GPR55 in the NAc plays a specific role in blocking nicotine-CPP behavior and might be a potential target for the treatment of nicotine use disorder.
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Registered trials
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