Perspectives on fronto-fugal circuitry from human imaging of alcohol use disorders

Zahr, Natalie M.; Pfefferbaum, Adolf; Sullivan, Edith V.

doi:10.1016/j.neuropharm.2017.01.018

Cited by 59 publications

(53 citation statements)

References 219 publications

(225 reference statements)

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“…Functional perturbation of the PFC has been consistently reported in alcohol use disorder and in animal models of EtOH exposure, which can lead to a shift toward less flexible behaviors mediated by subcortical structures (81)(82)(83). These shifts are thought to contribute to the progression from moderate drinking to uncontrolled, compulsive alcohol abuse.…”

Section: Discussionmentioning

confidence: 99%

Prefrontal Regulation of Punished Ethanol Self-administration

Halladay

Kocharian

Piantadosi

et al. 2020

Biological Psychiatry

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BACKGROUND: A clinical hallmark of alcohol use disorder is persistent drinking despite potential adverse consequences. The ventromedial prefrontal cortex (vmPFC) and dorsomedial prefrontal cortex (dmPFC) are positioned to exert top-down control over subcortical regions, such as the nucleus accumbens shell (NAcS) and basolateral amygdala, which encode positive and negative valence of ethanol (EtOH)-related stimuli. Prior rodent studies have implicated these regions in regulation of punished EtOH self-administration (EtOH-SA). METHODS: We conducted in vivo electrophysiological recordings in mouse vmPFC and dmPFC to obtain neuronal correlates of footshock-punished EtOH-SA. Ex vivo recordings were performed in NAcS D 1 receptor-expressing medium spiny neurons receiving vmPFC input to examine punishment-related plasticity in this pathway. Optogenetic photosilencing was employed to assess the functional contribution of the vmPFC, dmPFC, vmPFC projections to NAcS, or vmPFC projections to basolateral amygdala, to punished EtOH-SA. RESULTS: Punishment reduced EtOH lever pressing and elicited aborted presses (lever approach followed by rapid retraction). Neurons in the vmPFC and dmPFC exhibited phasic firing to EtOH lever presses and aborts, but only in the vmPFC was there a population-level shift in coding from lever presses to aborts with punishment. Closed-loop vmPFC, but not dmPFC, photosilencing on a postpunishment probe test negated the reduction in EtOH lever presses but not in aborts. Punishment was associated with altered plasticity at vmPFC inputs to D 1 receptorexpressing medium spiny neurons in the NAcS. Photosilencing vmPFC projections to the NAcS, but not to the basolateral amygdala, partially reversed suppression of EtOH lever presses on probe testing. CONCLUSIONS: These findings demonstrate a key role for the vmPFC in regulating EtOH-SA after punishment, with implications for understanding the neural basis of compulsive drinking in alcohol use disorder.

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Section: Discussionmentioning

confidence: 99%

Prefrontal Regulation of Punished Ethanol Self-administration

Halladay

Kocharian

Piantadosi

et al. 2020

Biological Psychiatry

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“…Neuroradiologically, the mainstay of studies of uncomplicated alcoholism concurs with neuropathological findings, especially of white matter involvement . Quantitative MRI studies report tissue shrinkage typically in the anterior superior vermis, involving lobules I‐V with additional sites of volume deficit in the white matter of the cerebellar hemispheres (; for review,), also exacerbated by common alcoholism‐related concomitant complications …”

Section: Introductionmentioning

confidence: 90%

Accelerated aging and motor control deficits are related to regional deformation of central cerebellar white matter in alcohol use disorder

et al. 2019

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The World Health Organization estimates a 12-month prevalence rate of 8+% for an alcohol use disorder (AUD) diagnosis in people age 15 years and older in the United States and Europe, presenting significant health risks that have the potential of accelerating age-related functional decline. According to neuropathological studies, white matter systems of the cerebellum are vulnerable to chronic alcohol dependence. To pursue the effect of AUD on white matter structure and functions in vivo, this study used T1-weighted, magnetic resonance imaging (MRI) to quantify the total corpus medullare of the cerebellum and a finely grained analysis of its surface in 135 men and women with AUD (mean duration of abstinence, 248 d) and 128 age-and sexmatched control participants; subsets of these participants completed motor testing.We identified an AUD-related volume deficit and accelerated aging in the total corpus medullare. Novel deformation-based surface morphometry revealed regional shrinkage of surfaces adjacent to lobules I-V, lobule IX, and vermian lobule X. In addition, accelerated aging was detected in the regional surface areas adjacent to lobules I-V, lobule VI, lobule VIIB, and lobules VIII, IX, and X. Sex differences were not identified for any measure. For both volume-based and surface-based analyses, poorer performance in gait and balance, manual dexterity, and grip strength were linked to greater regional white matter structural deficits. Our results suggest that local deformation of the corpus medullare has the potential of identifying structurally and functionally segregated networks affected in AUD.

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“…This assertion is supported by longitudinal evidence indicating that at least partial reversal of tissue volume deficits and ventricular dilatation occur early in abstinence-over days to weeks 6,7 -and that further cortical tissue shrinkage ensues with resumption of drinking. 1,8,9 The most commonly reported regions affected in vivo are frontally distributed, notably superior and middle lateral, orbital, and medial frontal gyri in individuals with treated [10][11][12] and never-treated 13 alcoholism. Prefrontal cortex is also a target of normal aging, showing pronounced volume decline from approximately age 50 years onward.…”

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confidence: 99%

The Role of Aging, Drug Dependence, and Hepatitis C Comorbidity in Alcoholism Cortical Compromise

et al. 2018

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Drug dependence and HCV infection compounded deleterious effects of alcohol dependence on frontal cortical volumes but could not account for the frontally distributed volume deficits in the drug-free participants with alcoholism. We speculate that age-alcohol interactions notable in frontal cortex put older adults at heightened risk for age-associated neurocompromise even if alcohol misuse is initiated later in life.

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Perspectives on fronto-fugal circuitry from human imaging of alcohol use disorders

Cited by 59 publications

References 219 publications

Prefrontal Regulation of Punished Ethanol Self-administration

Prefrontal Regulation of Punished Ethanol Self-administration

Accelerated aging and motor control deficits are related to regional deformation of central cerebellar white matter in alcohol use disorder

The Role of Aging, Drug Dependence, and Hepatitis C Comorbidity in Alcoholism Cortical Compromise

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