Effects of caffeine on ethanol-elicited place preference, place aversion and ERK phosphorylation in CD-1 mice.


Journal

Journal of psychopharmacology (Oxford, England)
ISSN: 1461-7285
Titre abrégé: J Psychopharmacol
Pays: United States
ID NLM: 8907828

Informations de publication

Date de publication:
12 2020
Historique:
pubmed: 27 10 2020
medline: 5 11 2021
entrez: 26 10 2020
Statut: ppublish

Résumé

Epidemiological studies indicate a rise in the combined consumption of caffeinated and alcoholic beverages, which can lead to increased risk of alcoholic-beverage overconsumption. However, the effects of the combination of caffeine and ethanol in animal models related to aspects of drug addiction are still underexplored. To characterize the pharmacological interaction between caffeine and ethanol and establish if caffeine can affect the ability of ethanol (2 g/kg) to elicit conditioned place preference and conditioned place aversion, we administered caffeine (3 or 15 mg/kg) to male CD-1 mice before saline or ethanol. Moreover, we determined if these doses of caffeine could affect ethanol (2 g/kg) elicited extracellular signal-regulated kinase phosphorylation in brain areas, nucleus accumbens, bed nucleus of stria terminalis, central nucleus of the amygdala, and basolateral amygdala, previously associated with this type of associative learning. In the place-conditioning paradigm, caffeine did not have an effect on its own, whereas ethanol elicited significant conditioned-place preference and conditioned-place aversion. Caffeine (15 mg/kg) significantly prevented the acquisition of ethanol-elicited conditioned-place preference and, at both doses, also prevented the acquisition of ethanol-elicited conditioned-place aversion. Moreover, both doses of caffeine also prevented ethanol-elicited extracellular signal-regulated kinase phosphorylation expression in all brain areas examined. The present data indicate a functional antagonistic action of caffeine and ethanol on associative learning and extracellular signal-regulated kinase phosphorylation after an acute interaction. These results could provide exciting grounds for further studies, also in a translational perspective, of their pharmacological interaction modulating other processes involved in drug consumption and addiction.

Sections du résumé

BACKGROUND
Epidemiological studies indicate a rise in the combined consumption of caffeinated and alcoholic beverages, which can lead to increased risk of alcoholic-beverage overconsumption. However, the effects of the combination of caffeine and ethanol in animal models related to aspects of drug addiction are still underexplored.
AIMS
To characterize the pharmacological interaction between caffeine and ethanol and establish if caffeine can affect the ability of ethanol (2 g/kg) to elicit conditioned place preference and conditioned place aversion, we administered caffeine (3 or 15 mg/kg) to male CD-1 mice before saline or ethanol. Moreover, we determined if these doses of caffeine could affect ethanol (2 g/kg) elicited extracellular signal-regulated kinase phosphorylation in brain areas, nucleus accumbens, bed nucleus of stria terminalis, central nucleus of the amygdala, and basolateral amygdala, previously associated with this type of associative learning.
RESULTS
In the place-conditioning paradigm, caffeine did not have an effect on its own, whereas ethanol elicited significant conditioned-place preference and conditioned-place aversion. Caffeine (15 mg/kg) significantly prevented the acquisition of ethanol-elicited conditioned-place preference and, at both doses, also prevented the acquisition of ethanol-elicited conditioned-place aversion. Moreover, both doses of caffeine also prevented ethanol-elicited extracellular signal-regulated kinase phosphorylation expression in all brain areas examined.
CONCLUSIONS
The present data indicate a functional antagonistic action of caffeine and ethanol on associative learning and extracellular signal-regulated kinase phosphorylation after an acute interaction. These results could provide exciting grounds for further studies, also in a translational perspective, of their pharmacological interaction modulating other processes involved in drug consumption and addiction.

Identifiants

pubmed: 33103552
doi: 10.1177/0269881120965892
doi:

Substances chimiques

Central Nervous System Depressants 0
Central Nervous System Stimulants 0
Caffeine 3G6A5W338E
Ethanol 3K9958V90M
Extracellular Signal-Regulated MAP Kinases EC 2.7.11.24

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1357-1370

Auteurs

Simona Porru (S)

Department of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.
Department of Psychobiology, University Jaume I, Castelló, Spain.

Riccardo Maccioni (R)

Department of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.

Valentina Bassareo (V)

Department of Biomedical Sciences, University of Cagliari, Monserrato, Italy.

Alessandra T Peana (AT)

Department of Chemistry and Pharmacy, University of Sassari, Sassari, Italy.

John D Salamone (JD)

Department of Psychological Sciences, University of Connecticut, Storrs, USA.

Mercè Correa (M)

Department of Psychobiology, University Jaume I, Castelló, Spain.

Elio Acquas (E)

Department of Life and Environmental Sciences, University of Cagliari, Monserrato, Italy.
Centre of Excellence on Neurobiology of Addiction, University of Cagliari, Cagliari, Italy.

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Classifications MeSH