Mutual assistance of nucleus accumbens cannabinoid receptor-1 and orexin receptor-2 in response to nicotine: a single-unit study.

AM251 Cannabinoid system Nicotine Nucleus accumbens Orexin system Single-unit recording

Journal

Research in pharmaceutical sciences

ISSN: 1735-5362

Titre abrégé: Res Pharm Sci

Pays: Iran

ID NLM: 101516968

Informations de publication

Date de publication:
Apr 2021

Historique:

received: 05 05 2020

revised: 22 08 2020

accepted: 24 01 2021

entrez: 4 6 2021

pubmed: 5 6 2021

medline: 5 6 2021

Statut: epublish

Résumé

The nucleus accumbens (NAc) express both orexin-2 receptor (OX2R) and cannabinoid receptor type 1 (CB1R). Orexin and cannabinoid regulate the addictive properties of nicotine. In this study, the effect of the CB1R blockade on the electrical activity of NAc neurons in response to nicotine, and its probable interaction with the OX2R in this event, within this area, were examined The spontaneous firing rate of NAc was initially recorded for 15 min, and then 5 min before subcutaneous injection of nicotine (0.5 mg/kg)/saline, AM251 and TCS-OX2-29 were injected into the NAc. Neuronal responses were recorded for 70 min, after nicotine administration. Nicotine excited the NAc neurons significantly and intra-NAc microinjection of AM251 (25 and 125 ng/rat), as a selective CB1R antagonist, prevented the nicotine-induced increases of NAc neuronal responses. Moreover, microinjection of AM251 (125 ng/rat), before saline injection, could not affect the percentage of change of the neuronal response. Finally, simultaneous intra-NAc administration of the effective or ineffective doses of AM251 and TCS-OX2-29 (a selective antagonist of OX2R) prevented the nicotine- induced increases of NAc neuronal responses, so that there was a significant difference between the group received ineffective doses of both antagonists and the AM251 ineffective dose. The results suggest that the CB1R can modulate the NAc reaction to the nicotine, and it can be concluded that there is a potential interplay between the OX2R and CB1R in the NAc, in relation to nicotine.

Sections du résumé

BACKGROUND AND PURPOSE OBJECTIVE

EXPERIMENTAL APPROACH METHODS

The spontaneous firing rate of NAc was initially recorded for 15 min, and then 5 min before subcutaneous injection of nicotine (0.5 mg/kg)/saline, AM251 and TCS-OX2-29 were injected into the NAc. Neuronal responses were recorded for 70 min, after nicotine administration.

FINDINGS/RESULTS RESULTS

Nicotine excited the NAc neurons significantly and intra-NAc microinjection of AM251 (25 and 125 ng/rat), as a selective CB1R antagonist, prevented the nicotine-induced increases of NAc neuronal responses. Moreover, microinjection of AM251 (125 ng/rat), before saline injection, could not affect the percentage of change of the neuronal response. Finally, simultaneous intra-NAc administration of the effective or ineffective doses of AM251 and TCS-OX2-29 (a selective antagonist of OX2R) prevented the nicotine- induced increases of NAc neuronal responses, so that there was a significant difference between the group received ineffective doses of both antagonists and the AM251 ineffective dose.

CONCLUSION AND IMPLICATIONS CONCLUSIONS

The results suggest that the CB1R can modulate the NAc reaction to the nicotine, and it can be concluded that there is a potential interplay between the OX2R and CB1R in the NAc, in relation to nicotine.

Identifiants

DOI: 10.4103/1735-5362.310524 PMID: 34084204 PMC: PMC8102922

pubmed: 34084204

doi: 10.4103/1735-5362.310524

pii: RPS-16-173

pmc: PMC8102922

doi:

Types de publication

Journal Article

Langues

eng

Pagination

173-181

Informations de copyright

Déclaration de conflit d'intérêts

All authors declared there is no conflict of interest in this study.

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