Sigma-1 antagonism inhibits binge ethanol drinking at adolescence.


Journal

Drug and alcohol dependence
ISSN: 1879-0046
Titre abrégé: Drug Alcohol Depend
Pays: Ireland
ID NLM: 7513587

Informations de publication

Date de publication:
01 10 2020
Historique:
received: 25 05 2020
revised: 14 07 2020
accepted: 23 07 2020
pubmed: 14 8 2020
medline: 13 3 2021
entrez: 14 8 2020
Statut: ppublish

Résumé

Ethanol use during adolescence is a significant health problem, yet the pharmacological treatments to reduce adolescent binge drinking are scarce. The present study assessed, in male and female adolescent Wistar rats, if the sigma-1 receptor (S1-R) antagonists S1RA or BD-1063 disrupted ethanol drinking. Three times a week, for two weeks, the rats received the S1-R antagonists. Thirty min later they were exposed, for 2 h, to a bottle of 8% or 10 % v/v ethanol. A 24 h, two-bottle, ethanol intake test was conducted after termination of these procedures. A subset of these rats was tested for recognition memory via the novel object recognition test. The rats given 64 mg/kg S1RA drank, in each binge session, significantly less than vehicle counterparts. Male rats given 4 or 16 mg/kg S1RA drank significantly less than those given 0 mg/kg in session 3 or in session 1 and 2, respectively; whereas female rats given 4 or 16 mg/kg drank significantly less than females given 0 mg/kg in session 2-5 or in sessions 2-6, respectively. Administration of 32 mg/kg, but not of 2 or 8 mg/kg, BD-1063 suppressed, across sessions, ethanol drinking. S1-R antagonism reduced absolute ethanol drinking at the two-bottle choice post-test. Recognition memory was not affected by the ethanol exposure. The results indicate that S1-R antagonists may be promising targets to prevent increases in ethanol intake at adolescence. The persistent effect of S1-R antagonism in free-choice drinking suggests that modulation of the S1-R is altering plastic effects associated with ethanol exposure.

Sections du résumé

BACKGROUND
Ethanol use during adolescence is a significant health problem, yet the pharmacological treatments to reduce adolescent binge drinking are scarce. The present study assessed, in male and female adolescent Wistar rats, if the sigma-1 receptor (S1-R) antagonists S1RA or BD-1063 disrupted ethanol drinking.
METHODS
Three times a week, for two weeks, the rats received the S1-R antagonists. Thirty min later they were exposed, for 2 h, to a bottle of 8% or 10 % v/v ethanol. A 24 h, two-bottle, ethanol intake test was conducted after termination of these procedures. A subset of these rats was tested for recognition memory via the novel object recognition test.
RESULTS
The rats given 64 mg/kg S1RA drank, in each binge session, significantly less than vehicle counterparts. Male rats given 4 or 16 mg/kg S1RA drank significantly less than those given 0 mg/kg in session 3 or in session 1 and 2, respectively; whereas female rats given 4 or 16 mg/kg drank significantly less than females given 0 mg/kg in session 2-5 or in sessions 2-6, respectively. Administration of 32 mg/kg, but not of 2 or 8 mg/kg, BD-1063 suppressed, across sessions, ethanol drinking. S1-R antagonism reduced absolute ethanol drinking at the two-bottle choice post-test. Recognition memory was not affected by the ethanol exposure.
CONCLUSIONS
The results indicate that S1-R antagonists may be promising targets to prevent increases in ethanol intake at adolescence. The persistent effect of S1-R antagonism in free-choice drinking suggests that modulation of the S1-R is altering plastic effects associated with ethanol exposure.

Identifiants

pubmed: 32791285
pii: S0376-8716(20)30379-3
doi: 10.1016/j.drugalcdep.2020.108214
pii:
doi:

Substances chimiques

Receptors, sigma 0
Ethanol 3K9958V90M

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

108214

Informations de copyright

Copyright © 2020 Elsevier B.V. All rights reserved.

Auteurs

Leandro Ruiz-Leyva (L)

Department of Pharmacology, Faculty of Medicine, University of Granada, Spain; Institute of Neuroscience, Biomedical Research Center (CIBM), University of Granada, Spain; Instituto de Investigación Biosanitaria (IBS), Granada, Spain.

Agustín Salguero (A)

Instituto de Investigación Médica M. y M. Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Córdoba, C.P. 5000, Argentina; Facultad de Psicología, Universidad Nacional de Córdoba, Córdoba, C.P. 5000, Argentina.

Ignacio Morón (I)

Department of Psychobiology and Centre of Investigation of Mind, Brain, and Behaviour (CIMCYC), University of Granada, Spain.

Enrique Portillo-Salido (E)

Drug Discovery and Preclinical Development, Esteve Pharmaceuticals, Parc Científic de Barcelona, Barcelona, Spain.

Cruz Miguel Cendán (CM)

Department of Pharmacology, Faculty of Medicine, University of Granada, Spain; Institute of Neuroscience, Biomedical Research Center (CIBM), University of Granada, Spain; Instituto de Investigación Biosanitaria (IBS), Granada, Spain. Electronic address: cmcendan@ugr.es.

Ricardo Marcos Pautassi (RM)

Instituto de Investigación Médica M. y M. Ferreyra (INIMEC-CONICET-Universidad Nacional de Córdoba), Córdoba, C.P. 5000, Argentina; Facultad de Psicología, Universidad Nacional de Córdoba, Córdoba, C.P. 5000, Argentina. Electronic address: ricardo.pautassi@unc.edu.ar.

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