Evidence map›Paper›PMID 23817165›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013

Role of CB2 cannabinoid receptors in the rewarding, reinforcing, and physical effects of nicotine.

Francisco Navarrete, Marta Rodríguez-Arias, Elena Martín-García, Daniela Navarro, María S García-Gutiérrez, María A Aguilar, Auxiliadora Aracil-Fernández, Pere Berbel, José Miñarro, Rafael Maldonado and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
9.0field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 118 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Review
  11. Review
  12. Review
  13. Endocannabinoid-Binding Receptors as Drug Targets.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  14. Review
  15. Review
  16. Review
  17. Article
  18. Review
  19. Review
  20. The CBInternational journal of molecular sciences · 2021
    Review

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 2 institutions in 1 country.

Francisco Navarrete1] Instituto de Neurociencias, Universidad Miguel Hernández (UMH)-CSIC, Alicante, Spain [2] Red Temática de Investigación Cooperativa en Salud (RETICS-Trastornos Adictivos), Instituto de Salud Carlos III, MICINN and FEDER, Madrid, Spain.
Marta Rodríguez-Arias
Elena Martín-García
Daniela Navarro
María S García-Gutiérrez
María A Aguilar
Auxiliadora Aracil-Fernández
Pere Berbel
José Miñarro
Rafael Maldonado
Jorge Manzanares
Instituto de Salud Carlos III · ESPompeu Fabra University · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

This study was aimed to evaluate the involvement of CB2 cannabinoid receptors (CB2r) in the rewarding, reinforcing and motivational effects of nicotine. Conditioned place preference (CPP) and intravenous self-administration experiments were carried out in knockout mice lacking CB2r (CB2KO) and wild-type (WT) littermates treated with the CB2r antagonist AM630 (1 and 3 mg/kg). Gene expression analyses of tyrosine hydroxylase (TH) and α3- and α4-nicotinic acetylcholine receptor subunits (nAChRs) in the ventral tegmental area (VTA) and immunohistochemical studies to elucidate whether CB2r colocalized with α3- and α4-nAChRs in the nucleus accumbens and VTA were performed. Mecamylamine-precipitated withdrawal syndrome after chronic nicotine exposure was evaluated in CB2KO mice and WT mice treated with AM630 (1 and 3 mg/kg). CB2KO mice did not show nicotine-induced place conditioning and self-administered significantly less nicotine. In addition, AM630 was able to block (3 mg/kg) nicotine-induced CPP and reduce (1 and 3 mg/kg) nicotine self-administration. Under baseline conditions, TH, α3-nAChR, and α4-nAChR mRNA levels in the VTA of CB2KO mice were significantly lower compared with WT mice. Confocal microscopy images revealed that CB2r colocalized with α3- and α4-nAChRs. Somatic signs of nicotine withdrawal (rearings, groomings, scratches, teeth chattering, and body tremors) increased significantly in WT but were absent in CB2KO mice. Interestingly, the administration of AM630 blocked the nicotine withdrawal syndrome and failed to alter basal behavior in saline-treated WT mice. These results suggest that CB2r play a relevant role in the rewarding, reinforcing, and motivational effects of nicotine. Pharmacological manipulation of this receptor deserves further consideration as a potential new valuable target for the treatment of nicotine dependence.

Indexed as

Reinforcement, PsychologyRewardAnimalsConditioning, OperantMaleMiceMice, KnockoutNicotineNucleus AccumbensReceptor, Cannabinoid, CB2Self AdministrationSubstance Withdrawal SyndromeVentral Tegmental AreaNicotineReceptor, Cannabinoid, CB2

Identifiers

PMID23817165
PMCPMC3799072
OpenAlexW2085163003

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.