mTORC1 pathway is involved in the kappa opioid receptor activation-induced increase in excessive alcohol drinking in mice.


Journal

Pharmacology, biochemistry, and behavior
ISSN: 1873-5177
Titre abrégé: Pharmacol Biochem Behav
Pays: United States
ID NLM: 0367050

Informations de publication

Date de publication:
08 2020
Historique:
received: 27 01 2020
revised: 22 05 2020
accepted: 25 05 2020
pubmed: 30 5 2020
medline: 9 2 2021
entrez: 30 5 2020
Statut: ppublish

Résumé

KOP-r agonist U50,488H produces strong aversion and anxiety/depression-like behaviors that enhance alcohol intake and promote alcohol seeking and relapse-like drinking in rodents. Mammalian target of rapamycin complex 1 (mTORC1) pathway in mouse striatum is highly involved in excessive alcohol intake and seeking, and in the U50,488H-induced conditioned place aversion. Therefore, we hypothesized that KOP-r activation increases alcohol consumption through the mTORC1 activation. This study focuses on: (1) how chronic excessive alcohol drinking (4-day drinking-in-the-dark paradigm followed by 3-week chronic intermittent access drinking paradigm [two-bottle choice, 24-h access every other day]) affected nuclear transcript levels of the mTORC1 pathway genes in mouse nucleus accumbens shell (NAcs), using transcriptome-wide RNA sequencing analysis; and (2) whether selective mTORC1 inhibitor rapamycin could alter excessive alcohol drinking and prevent U50,488H-promoted alcohol intake. Thirteen nuclear transcripts of mTORC1 pathway genes showed significant up-regulation in the NAcs, with two genes down-regulated, after excessive alcohol drinking, suggesting the mTORC1 pathway was profoundly disrupted. Single administration of rapamycin decreased alcohol drinking in a dose-dependent manner. U50,488H increased alcohol drinking, and pretreatment with rapamycin, at a dose lower than effective doses, blocked the U50,488H-promoted alcohol intake in a dose-dependent manner, indicating a mTORC1-mediated mechanism. Our results provide supportive and direct evidence relevant to the transcriptional profiling of the critical mTORC1 genes in mouse NAc shell: with functional and pharmacological effects of rapamycin, altered nuclear transcripts in the mTORC1 signaling pathway after excessive alcohol drinking may contribute to increased alcohol intake triggered by KOP-r activation.

Identifiants

pubmed: 32470351
pii: S0091-3057(20)30053-8
doi: 10.1016/j.pbb.2020.172954
pmc: PMC7442164
mid: NIHMS1609471
pii:
doi:

Substances chimiques

Central Nervous System Depressants 0
Receptors, Opioid, kappa 0
Ethanol 3K9958V90M
3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cyclohexyl)-benzeneacetamide, (trans)-Isomer 67198-13-4
Mechanistic Target of Rapamycin Complex 1 EC 2.7.11.1
Sirolimus W36ZG6FT64

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

172954

Subventions

Organisme : NIAAA NIH HHS
ID : R03 AA021970
Pays : United States

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of competing interest All authors declare that they have no conflicts of interest.

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Auteurs

Yan Zhou (Y)

Laboratory of the Biology of Addictive Diseases, The Rockefeller University, NY, USA. Electronic address: zhouya@rockefeller.edu.

Yupu Liang (Y)

Research Bioinformatics, CCTS, The Rockefeller University, NY, USA.

Mary Jeanne Kreek (MJ)

Laboratory of the Biology of Addictive Diseases, The Rockefeller University, NY, USA.

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Classifications MeSH