Alcohol Dependence Is Associated with Blunted Dopamine Transmission in the Ventral Striatum

Martínez, Diana; Gil, Roberto; Slifstein, Mark; Hwang, Dah‐Ren; Huang, Yiyun; Perez, Audrey; Kegeles, Lawrence S.; Talbot, Peter S.; Evans, Suzette M.; Krystal, John H.; Laruelle, Marc; Abi‐Dargham, Anissa

doi:10.1016/j.biopsych.2005.04.044

Cited by 404 publications

(308 citation statements)

References 43 publications

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“…For example, decreased ventral striatal dopamine release and insensitivity to this release has been implicated in AD as a mechanism that impairs the ability to develop an adaptive behavior to abstain from drinking (77)(78)(79). Dopamine is a substrate of MAO-A, and in the present study elevated MAO-A V T was found in the ventral striatum.…”

Section: Discussionsupporting

confidence: 54%

Greater Monoamine Oxidase A Binding in Alcohol Dependence

Matthews

Kish

et al. 2014

Biological Psychiatry

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Background-Alcohol dependence (AD) is a multiorgan disease in which excessive oxidative stress and apoptosis are implicated. Monoamine oxidase A (MAO-A) is an important enzyme on the outer mitochondrial membrane that participates in the cellular response to oxidative stress and mitochondrial toxicity. It is unknown whether MAO-A levels are abnormal in AD. We hypothesized that MAO-A V T , an index of MAO-A level, is elevated in the prefrontal cortex (PFC) during AD, because markers of greater oxidative stress and apoptosis are reported in the brain in AD and a microarray analysis reported greater MAO-A messenger RNA in the PFC of rodents exposed to alcohol vapor.

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Section: Discussionsupporting

confidence: 54%

Greater Monoamine Oxidase A Binding in Alcohol Dependence

Matthews

Kish

et al. 2014

Biological Psychiatry

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“…A downregulation of NAcc sensitivity in consequence of these mood states could explain the observed lower reactivity of the NAcc-despite a tendency of higher functional connectivity between NAcc and VTA. The idea of blunted neural responses toward reward has also been proposed for addictive disorders (Martinez et al, 2005;Volkow et al, 2010). However, this interpretation should be taken with care, because our cross-sectional study design does not allow for more specific conclusions.…”

Section: Reward Processing In Ud and Bdmentioning

confidence: 94%

Reward Processing in Unipolar and Bipolar Depression: A Functional MRI Study

Redlich

Dohm

Grotegerd

et al. 2015

Neuropsychopharmacol

138

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Differentiating bipolar disorders (BD) from unipolar depression (UD) remains a major clinical challenge. The identification of neurobiological markers may help to differentiate these disorders, particularly during depressive episodes. This cross-sectional study, including 33 patients with UD, 33 patients with BD, and 34 healthy controls, is one of the first to directly compare UD and BD with respect to reward processing. A card-guessing paradigm was employed and brain activity associated with reward processing was investigated by means of fMRI. A 3 (group) × 2 (condition: reward4control, loss4control) ANOVA was conducted using the nucleus accumbens (NAcc) as ROI. Furthermore, a whole-brain approach was applied. A functional connectivity analysis was performed to characterize diagnosis-related alterations in the functional coupling between the NAcc and other brain areas. The ANOVA revealed higher activity for healthy controls (HCs) than for BD and UD in the NAcc during reward processing. Moreover, UD showed a higher functional connectivity between the NAcc and the VTA than HC. The patients groups could be differentiated in that BD showed a decreased activation, in the reward condition, of the NAcc, caudate nucleus, thalamus, putamen, insula, and prefrontal areas compared with UD. These results may help to refine the understanding of neural correlates of reward processing in both disorders, and to understand the neural underpinnings of anhedonia, a core symptom of depressive episodes.

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“…In addition, drug abusers (cocaine and alcohol) also show decreased DA release, which is likely to reflect reduced DA cell firing (Volkow et al 1997;Martinez et al 2005). DA release was measured using PET and [ 11 C]raclopride, which is a D 2 receptor radioligand that competes with endogenous DA for binding to D 2 receptors and thus can be used to assess the changes in DA induced by drugs.…”

Section: Reward/saliency Circuitry In Addiction and Obesitymentioning

confidence: 99%

Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology

Volkow

Wang

Fowler

et al. 2008

Phil. Trans. R. Soc. B

698

539

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Drugs and food exert their reinforcing effects in part by increasing dopamine (DA) in limbic regions, which has generated interest in understanding how drug abuse/addiction relates to obesity. Here, we integrate findings from positron emission tomography imaging studies on DA's role in drug abuse/addiction and in obesity and propose a common model for these two conditions. Both in abuse/addiction and in obesity, there is an enhanced value of one type of reinforcer (drugs and food, respectively) at the expense of other reinforcers, which is a consequence of conditioned learning and resetting of reward thresholds secondary to repeated stimulation by drugs (abuse/addiction) and by large quantities of palatable food (obesity) in vulnerable individuals (i.e. genetic factors). In this model, during exposure to the reinforcer or to conditioned cues, the expected reward (processed by memory circuits) overactivates the reward and motivation circuits while inhibiting the cognitive control circuit, resulting in an inability to inhibit the drive to consume the drug or food despite attempts to do so. These neuronal circuits, which are modulated by DA, interact with one another so that disruption in one circuit can be buffered by another, which highlights the need of multiprong approaches in the treatment of addiction and obesity.

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Alcohol Dependence Is Associated with Blunted Dopamine Transmission in the Ventral Striatum

Cited by 404 publications

References 43 publications

Greater Monoamine Oxidase A Binding in Alcohol Dependence

Greater Monoamine Oxidase A Binding in Alcohol Dependence

Reward Processing in Unipolar and Bipolar Depression: A Functional MRI Study

Overlapping neuronal circuits in addiction and obesity: evidence of systems pathology

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