Dopamine receptor agonists modulate voluntary alcohol intake independently of individual levels of alcohol intake in rats.

Marcia Spoelder,Louk J M J Vanderschuren,Annemarie M Baars,Marthe D Rotte,Heidi M B Lesscher

doi:10.1007/s00213-016-4330-x

Marcia Spoelder, Louk J M J Vanderschuren + Show 3 more

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https://doi.org/10.1007/s00213-016-4330-x

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Journal: Psychopharmacology	Publication Date: May 28, 2016
Citations: 8	License type: CC BY 4.0

Affiliation: Utrecht University

Abstract

RationaleIndividual susceptibility to alcohol use disorder has been related to functional changes in dopaminergic neurotransmission.ObjectivesThe aim of the current work was to assess the effects of selective dopamine D1 and D2 receptor agonists and antagonists on alcohol consumption in rats that differ in individual levels of alcohol intake.MethodsThe effects of the dopamine D1 receptor agonist SKF 82958, the dopamine D1 receptor antagonist SCH 23390, the dopamine D2 receptor agonist sumanirole and the dopamine D2 receptor antagonist L741,626 on alcohol consumption and preference were assessed at different time points after treatment in subgroups of low and high alcohol drinking rats (LD and HD) using an intermittent alcohol access paradigm.ResultsSKF 82958 decreased alcohol intake and alcohol preference throughout the 24-h session. Sumanirole decreased alcohol intake during the first 2 h, but increased alcohol intake during the remainder of the session. The effects of SKF 82958 and sumanirole on alcohol intake and alcohol preference were comparable in LD and HD. By contrast, the dopamine receptor antagonists SCH 23390 and L741,626 did not alter alcohol consumption in either group at any time point.ConclusionsThese data indicate that stimulation of dopamine D1 receptors reduces alcohol intake, but that endogenous dopamine does not play a primary role in alcohol consumption. Moreover, the difference in alcohol consumption between LD and HD does not involve altered dopamine signaling.

Highlights

Alcohol use disorder (AUD) is a chronic relapsing brain disorder, which is characterized by compulsive engagement in alcohol use (American Psychiatric Association 2013)
low alcohol drinking (LD) typically became more pronounced as the session progressed
Preference for alcohol was greater in HD than LD

Summary

Introduction

Alcohol use disorder (AUD) is a chronic relapsing brain disorder, which is characterized by compulsive engagement in alcohol use (American Psychiatric Association 2013). More insight into the mechanisms underlying individual variation in alcohol consumption may provide important knowledge about the development of AUD, which may contribute to improved personalized treatments for AUD. One prominent hypothesis is that variations in dopaminergic neurotransmission underlie the individual susceptibility to AUD (Noble 2000; Tupala and Tiihonen 2004; Le Foll et al 2009). Acute alcohol administration has been shown to activate dopamine neuron firing in the ventral tegmental area (VTA) (Gessa et al 1985; Brodie et al 1990; Brodie et al 1999), and alcohol ingestion increases dopamine release in the ventral striatum (Weiss et al 1993; Boileau et al 2003; Doyon et al 2003).

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