Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers

Kareken, David A.; Bragulat, Veronique; Džemidžić, Mario; Cox, Cari; Talavage, Thomas M.; Davidson, Dena; O’Connor, Sean

doi:10.1016/j.neuroimage.2009.11.076

Cited by 73 publications

(103 citation statements)

References 78 publications

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“…If alcohol consumption is at least partially mediated by palatability, the release of endogenous MOR ligands would be expected to promote further consumption. In keeping with this hypothesis, recent data indicate that an alcohol infusion, which bypasses gustatory mechanisms, does not alter blood oxygen leveldependent (BOLD) signal in the OFC of either subjects with a family history of alcoholism or matched controls (13). Although our data are consistent with the idea that drinking alcohol induces endogenous opioid release in the OFC, our study cannot distinguish between the contributions of the characteristic taste and smell of alcohol and a direct action of alcohol on the brain.…”

Section: Discussionmentioning

confidence: 90%

Alcohol Consumption Induces Endogenous Opioid Release in the Human Orbitofrontal Cortex and Nucleus Accumbens

et al. 2012

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Excessive consumption of alcohol is among the leading causes of preventable death worldwide. Although ethanol modulates a variety of molecular targets, including several neurotransmitter receptors, the neural mechanisms that underlie its rewarding actions and lead to excessive consumption are unknown. Studies in animals suggest that release of endogenous opioids by ethanol promotes further consumption. To examine this issue in humans and to determine where in the brain endogenous opioids act to promote alcohol consumption, we measured displacement of a radiolabeled μ opioid receptor agonist, [¹¹C]carfentanil, before and immediately after alcohol consumption in both heavy drinkers and control subjects. Drinking alcohol induced opioid release in the nucleus accumbens and orbitofrontal cortex, areas of the brain implicated in reward valuation. Opioid release in the orbitofrontal cortex and nucleus accumbens was significantly positively correlated. Furthermore, changes in orbitofrontal cortex binding correlated significantly with problem alcohol use and subjective high in heavy drinkers, suggesting that differences in endogenous opioid function in these regions contribute to excessive alcohol consumption. These results also suggest a possible mechanism by which opioid antagonists such as naltrexone act to treat alcohol abuse.

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Section: Discussionmentioning

confidence: 90%

Alcohol Consumption Induces Endogenous Opioid Release in the Human Orbitofrontal Cortex and Nucleus Accumbens

et al. 2012

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“…In that context, FHP subjects had the most robust VST DA release, which is consistent with other human imaging studies in which familial alcoholism modulates brain activation to alcohol cues. For instance, we (Kareken et al, 2010) and others (Tapert et al, 2003) have demonstrated that alcoholassociated cues differentially activate the medial prefrontal cortex (which sends axonal projections to the VST; for review see Haber and Knutson, 2010) as a function of FH. In contrast, an fMRI study of children of alcoholics did not detect a difference in VST activation for monetary rewards (Bjork et al, 2008), while another study of FHP subjects found reduced VST activation to monetary rewards compared with FHN subjects (Andrews et al, 2011).…”

Section: Discussionmentioning

confidence: 96%

“…In particular, Weiss et al, 1993 found that rats selectively bred for high alcohol drinking showed a larger ventral striatal DA response to alcohol taste and intoxication than nonselected rats, suggesting that the genetic propensity for alcohol use disorders (AUD) is linked to differential striatal DA function. Two human studies found that, in subjects with a family history (FH) of alcoholism, the medial prefrontal cortex (which sends axonal projections to the striatum; Haber and Knutson, 2010), is activated more strongly in response to alcohol cues relative to family history-negative controls (Tapert et al, 2003;Kareken et al, 2010). Cue-elicited DA transmission may also relate to alcohol preference, as nonselected rats with the highest ethanol preference showed the largest increase in ventral striatal DA release in response to oral contact with alcohol (Doyon et al, 2005).…”

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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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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“…Ventromedial and medial prefrontal cortices are regions where neuronal activity varies as a function of the perceived reward value of stimuli (Hare, et al, 2009; Hare et al, 2008; Kable & Glimcher, 2007). Our laboratory has accordingly demonstrated that both alcoholic drink (Bragulat et al, 2008; Kareken et al, 2010a; Kareken et al, 2010b) and food aromas (Bragulat et al, 2010) robustly activate these medial frontal regions.…”

Section: Introductionmentioning

confidence: 97%

Correlation Between Ventromedial Prefrontal Cortex Activation to Food Aromas and Cue-Driven Eating: An fMRI Study

et al. 2012

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Food aromas are signals associated with both food's availability and pleasure. Previous research from this laboratory has shown that food aromas under fasting conditions evoke robust activation of medial prefrontal brain regions thought to reflect reward value (Bragulat, et al. 2010). In the current study, eighteen women (eleven normal-weight and seven obese) underwent a two-day imaging study (one after being fed, one while fasting). All were imaged on a 3T Siemens Trio-Tim scanner while sniffing two food (F; pasta and beef) odors, one non-food (NF; Douglas fir) odor, and an odorless control (CO). Prior to imaging, participants rated hunger and perceived odor qualities, and completed the Dutch Eating Behavior Questionnaire (DEBQ) to assess “Externality” (the extent to which eating is driven by external food cues). Across all participants, both food and non-food odors (compared to CO) elicited large blood oxygenation level dependent (BOLD) responses in olfactory and reward-related areas, including the medial prefrontal and anterior cingulate cortex, bilateral orbitofrontal cortex, and bilateral piriform cortex, amygdala, and hippocampus. However, food odors produced greater activation of medial prefrontal cortex, left lateral orbitofrontal cortex and inferior insula than non-food odors. Moreover, there was a significant correlation between the [F > CO] BOLD response in ventromedial prefrontal cortex and “Externality” sub-scale scores of the DEBQ, but only under the fed condition; no such correlation was present with the [NF > CO] response. This suggests that in those with high Externality, ventromedial prefrontal cortex may inappropriately valuate external food cues in the absence of internal hunger.

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Family history of alcoholism mediates the frontal response to alcoholic drink odors and alcohol in at-risk drinkers

Cited by 73 publications

References 78 publications

Alcohol Consumption Induces Endogenous Opioid Release in the Human Orbitofrontal Cortex and Nucleus Accumbens

Alcohol Consumption Induces Endogenous Opioid Release in the Human Orbitofrontal Cortex and Nucleus Accumbens

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

Correlation Between Ventromedial Prefrontal Cortex Activation to Food Aromas and Cue-Driven Eating: An fMRI Study

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