Dopamine Activity in the Nucleus Accumbens During Consummatory Phases of Oral Ethanol Self‐Administration

Doyon, William M.; York, Jennifer; Diaz, Laurea M.; Samson, Herman H.; Czachowski, Cristine L.; Gonzales, Rueben A.

doi:10.1097/01.alc.0000089959.66222.b8

Cited by 143 publications

(151 citation statements)

References 42 publications

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“…Ramchandani et al, 2011), we believe that alcohol-conditioned taste cues alone may also be sufficient to induce ventral striatal DA release-an interpretation consistent with findings in animals (Doyon et al, 2003;Doyon et al, 2005). Although ethanol can directly excite ventral tegmental DA neurons in vitro (Brodie et al, 1999), alcoholconditioned cues can alone provoke VST DA responses in behaving animals that are reflective of motivated behavior and alcohol-seeking (Gonzales et al, 2004).…”

Section: Discussionsupporting

confidence: 81%

“…While the DA effects in these studies were attributed to alcohol intoxication, animal studies indicate that alcohol-related taste cues may alone elicit DA release. Two studies demonstrate that ventral striatal DA peaks upon oral contact with ethanol, before the rise of alcohol concentration in the brain (Doyon et al, 2005;Doyon et al, 2003). This suggests that alcohol's taste or other orosensory cues are potent triggers for ventral striatal DA release, and that the DA release from oral alcohol in human studies could be attributed (at least in part) to a beverage's intraoral sensory cues.…”

Section: Introductionmentioning

confidence: 99%

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Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism

Oberlin

Džemidžić

Tran

et al. 2013

Neuropsychopharmacol

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Striatal dopamine (DA) is increased by virtually all drugs of abuse, including alcohol. However, drug-associated cues are also known to provoke striatal DA transmission-a phenomenon linked to the motivated behaviors associated with addiction. To our knowledge, no one has tested if alcohol's classically conditioned flavor cues, in the absence of a significant pharmacologic effect, are capable of eliciting striatal DA release in humans. Employing positron emission tomography (PET), we hypothesized that beer's flavor alone can reduce the binding potential (BP) of [ 11 C]raclopride (RAC; a reflection of striatal DA release) in the ventral striatum, relative to an appetitive flavor control. Forty-nine men, ranging from social to heavy drinking, mean age 25, with a varied family history of alcoholism underwent two [ 11 C]RAC PET scans: one while tasting beer, and one while tasting Gatorade. Relative to the control flavor of Gatorade, beer flavor significantly increased self-reported desire to drink, and reduced [ 11 C]RAC BP, indicating that the alcohol-associated flavor cues induced DA release. BP reductions were strongest in subjects with first-degree alcoholic relatives. These results demonstrate that alcoholconditioned flavor cues can provoke ventral striatal DA release, absent significant pharmacologic effects, and that the response is strongest in subjects with a greater genetic risk for alcoholism. Striatal DA responses to salient alcohol cues may thus be an inherited risk factor for alcoholism.

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Section: Discussionsupporting

confidence: 81%

Section: Introductionmentioning

confidence: 99%

Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism

Oberlin

Džemidžić

Tran

et al. 2013

Neuropsychopharmacol

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“…The reward value of ethanol appears to be regulated by activation of dopamine cell fi ring in the ventral tegmental area (VTA), which projects to the nucleus accumbens (NAc) (Appel et al, 2006;Doyon et al, 2003Doyon et al, , 2005Robinson et al, 2009). Manipulating the fi ring rate of dopamine neurons either directly (Bass et al 2013) or indirectly via changes in γ-aminobutyric acid (GABA) neuronal activity in the VTA (Anstee et al, 2013;Mitchell et al, 2014) can alter ethanol intake.…”

Section: Discussionmentioning

confidence: 99%

Intermittent High-Dose Ethanol Exposure Increases Ethanol Preference in Rats

Peris¹,

Rhodes²,

McCullough³

et al. 2015

J. Stud. Alcohol Drugs

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ABSTRACT. Objective: Alcohol use disorders have both high social and economic costs and are among the leading causes of preventable death in the United States. Understanding the factors that contribute to escalation of alcohol intake is important in developing effective treatments for this problem. This study further characterizes the effects of limited intermittent exposure to high levels of alcohol on the preference for alcohol consumption over other incentives. Method: Fourteen male, Sprague-Dawley rats were trained to consume ethanol in a gelatin vehicle. They were then given free access to both ethanol gelatin and plain gelatin during daily choice periods interspersed with nonchoice periods (only plain gelatin access). After baseline ethanol preference was established, half of the rats were given eight injections of 3 g/kg ethanol during nonchoice periods (spread out over about 2 months), and the other half received saline injections. Ethanol preference was measured during subsequent choice periods. Results: Intermittent ethanol injections increased ethanol preference from 21% (SEM = 2.3%) of their total gelatin consumption during the fi rst choice period to 46.8% (SEM = 3.4%) during the third choice period. The saline-treated rats had no signifi cant change in ethanol preference. In addition, the ethanoltreated rats exhibited higher ethanol intake than saline-treated rats when ethanol gelatin was the only choice available. Conclusions: The results indicate that intermittent exposure to sedative doses of ethanol leads to an increased ethanol preference in rats. This suggests that occasional high-dose alcohol exposure could be an important contributor to the development of enhanced ethanol intake, which may affect the incidence of chronic alcoholism. (J. Stud. Alcohol Drugs, 76, 165-173, 2015)

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“…In the limbic circuit, the NAC, the VP (ventral pallidum), and the prefrontal cortex are known to be involved in ethanol reinforcement (Bassareo et al, 2003;Doyon et al, 2003;Samson and Czachowski, 2003). The limbic areas of the prefrontal cortex activate the STN, either by a direct excitatory input (the so-called 'hyperdirect pathway') or by an indirect disinhibitory pathway linking the NAC core and the STN via the VP (Maurice et al, 1998a, b).…”

Section: Discussionmentioning

confidence: 99%

Alcohol Preference Influences the Subthalamic Nucleus Control on Motivation for Alcohol in Rats

Lardeux

Baunez

2007

Neuropsychopharmacol

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In addition to its role in motor and attentional processes, the subthalamic nucleus (STN) has also been recently demonstrated to be involved in motivational function. Indeed, bilateral STN lesions modulate differentially the motivation for natural rewards and drugs of abuse, increasing motivation for food and decreasing motivation for cocaine in rats. Here, we show that in outbred rats, the STN can modulate the motivation for alcohol according to alcohol preference, without affecting alcohol intake. When performed on 'HighDrinker' rats, STN lesions enhanced the breaking point (BP) under a progressive ratio schedule of reinforcement and increased the time spent in the environment previously paired with alcohol access in the place preference paradigm. In contrast, when performed on 'Low-Drinker' rats, STN lesions decreased the BP and increased the time spent in the environment paired with water. These results show that STN lesions enhance the motivation for alcohol in rats showing a high alcohol preference, whereas they decrease it in rats showing a low preference for alcohol. These results suggest that the STN plays a complex role in the reward circuit, that is not limited to a dissociation between motivation for natural rewards and drugs of abuse, but takes other factors, such as alcohol preference, into account.

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Dopamine Activity in the Nucleus Accumbens During Consummatory Phases of Oral Ethanol Self‐Administration

Cited by 143 publications

References 42 publications

Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism

Beer Flavor Provokes Striatal Dopamine Release in Male Drinkers: Mediation by Family History of Alcoholism

Intermittent High-Dose Ethanol Exposure Increases Ethanol Preference in Rats

Alcohol Preference Influences the Subthalamic Nucleus Control on Motivation for Alcohol in Rats

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