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Disordered gambling: the evolving concept of behavioral addiction.

Clark L - Ann. N. Y. Acad. Sci. (2014)

Bottom Line: The similarities between gambling disorder and the substance use disorders have been well documented.As gambling is unlikely to exert actively damaging effects on the brain, the cognitive sequelae of gambling disorder may provide insights into addictive vulnerabilities; this idea is critically evaluated in light of recent structural imaging data.The relative potency of drug and nondrug rewards is considered, alongside evidence that cognitive distortions in the processing of chance (for example, the illusion of control and the gambler's fallacy) may constitute an important added ingredient in gambling.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, Centre for Gambling Research, University of British Columbia, Vancouver, Canada.

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Using PET with the [11C]raclopride ligand, we compared baseline binding as a marker of dopamine D2/D3 receptor availability in nine males with gambling disorder against nine male healthy participants. We detected no group difference in binding potential in regions of interest encompassing the overall striatum or the limbic subdivision that includes the nucleus accumbens. A representative image from one participant (a healthy control) is shown centrally, illustrating the striatal localization of raclopride binding. Despite the absence of a group difference, raclopride binding within the gamblers was negatively related with trait-impulsivity levels, on a measure of mood-related impulsivity (urgency) that shows robust group differences between gambling disorder and controls.85 Data redrawn from Ref. 51.
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fig01: Using PET with the [11C]raclopride ligand, we compared baseline binding as a marker of dopamine D2/D3 receptor availability in nine males with gambling disorder against nine male healthy participants. We detected no group difference in binding potential in regions of interest encompassing the overall striatum or the limbic subdivision that includes the nucleus accumbens. A representative image from one participant (a healthy control) is shown centrally, illustrating the striatal localization of raclopride binding. Despite the absence of a group difference, raclopride binding within the gamblers was negatively related with trait-impulsivity levels, on a measure of mood-related impulsivity (urgency) that shows robust group differences between gambling disorder and controls.85 Data redrawn from Ref. 51.

Mentions: Of course, fMRI provides only an indirect measure of dopamine transmission, and other work has used positron emission tomography (PET) with dopamine radioligands like [11C]raclopride. Reduced striatal dopamine D2 receptor binding is a robust effect in individuals with drug addictions; this has been observed across stimulant,46 heroin,47 alcohol,48 and nicotine dependence,49 as well as in preclinical models of high impulsivity.50 Thus, there was a strong prediction that individuals with gambling disorder should display the same effect. Surprisingly, four independent PET studies to date have failed to detect any group differences in baseline (i.e., resting) dopamine D2 receptor availability in gambling disorder,51–54 although individual differences were seen as functions of impulsivity markers51 and symptom severity54 (Fig.1). Returning to the first question of neurotoxicity, a plausible inference is that the effects described in drug addiction are more reflective of drug-induced changes as opposed to preexisting vulnerability. Of greatest interest, a recent study has quantified dopamine release in gambling disorder, using a different ligand, [11C] (+)-4-propyl-9-hydroxynaphthoxazine (PHNO), in combination with amphetamine challenge.55 Previous studies in stimulant addicts consistently reported blunted dopamine release,56,57 but in a group of 12 males with gambling disorder, dopamine release in the dorsal striatum was increased relative to healthy males. The dopamine response to amphetamine was positively predicted by the baseline PHNO binding in the substantia nigra, which is thought to specifically reflect dopamine D3 receptor levels, and it was also correlated with symptom severity.55 In summary, the PET work in gambling disorder points to clear perturbations in dopamine transmission, but this is one area where the emerging profile in gambling disorder increasingly diverges from the established picture in drug addiction.


Disordered gambling: the evolving concept of behavioral addiction.

Clark L - Ann. N. Y. Acad. Sci. (2014)

Using PET with the [11C]raclopride ligand, we compared baseline binding as a marker of dopamine D2/D3 receptor availability in nine males with gambling disorder against nine male healthy participants. We detected no group difference in binding potential in regions of interest encompassing the overall striatum or the limbic subdivision that includes the nucleus accumbens. A representative image from one participant (a healthy control) is shown centrally, illustrating the striatal localization of raclopride binding. Despite the absence of a group difference, raclopride binding within the gamblers was negatively related with trait-impulsivity levels, on a measure of mood-related impulsivity (urgency) that shows robust group differences between gambling disorder and controls.85 Data redrawn from Ref. 51.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4285202&req=5

fig01: Using PET with the [11C]raclopride ligand, we compared baseline binding as a marker of dopamine D2/D3 receptor availability in nine males with gambling disorder against nine male healthy participants. We detected no group difference in binding potential in regions of interest encompassing the overall striatum or the limbic subdivision that includes the nucleus accumbens. A representative image from one participant (a healthy control) is shown centrally, illustrating the striatal localization of raclopride binding. Despite the absence of a group difference, raclopride binding within the gamblers was negatively related with trait-impulsivity levels, on a measure of mood-related impulsivity (urgency) that shows robust group differences between gambling disorder and controls.85 Data redrawn from Ref. 51.
Mentions: Of course, fMRI provides only an indirect measure of dopamine transmission, and other work has used positron emission tomography (PET) with dopamine radioligands like [11C]raclopride. Reduced striatal dopamine D2 receptor binding is a robust effect in individuals with drug addictions; this has been observed across stimulant,46 heroin,47 alcohol,48 and nicotine dependence,49 as well as in preclinical models of high impulsivity.50 Thus, there was a strong prediction that individuals with gambling disorder should display the same effect. Surprisingly, four independent PET studies to date have failed to detect any group differences in baseline (i.e., resting) dopamine D2 receptor availability in gambling disorder,51–54 although individual differences were seen as functions of impulsivity markers51 and symptom severity54 (Fig.1). Returning to the first question of neurotoxicity, a plausible inference is that the effects described in drug addiction are more reflective of drug-induced changes as opposed to preexisting vulnerability. Of greatest interest, a recent study has quantified dopamine release in gambling disorder, using a different ligand, [11C] (+)-4-propyl-9-hydroxynaphthoxazine (PHNO), in combination with amphetamine challenge.55 Previous studies in stimulant addicts consistently reported blunted dopamine release,56,57 but in a group of 12 males with gambling disorder, dopamine release in the dorsal striatum was increased relative to healthy males. The dopamine response to amphetamine was positively predicted by the baseline PHNO binding in the substantia nigra, which is thought to specifically reflect dopamine D3 receptor levels, and it was also correlated with symptom severity.55 In summary, the PET work in gambling disorder points to clear perturbations in dopamine transmission, but this is one area where the emerging profile in gambling disorder increasingly diverges from the established picture in drug addiction.

Bottom Line: The similarities between gambling disorder and the substance use disorders have been well documented.As gambling is unlikely to exert actively damaging effects on the brain, the cognitive sequelae of gambling disorder may provide insights into addictive vulnerabilities; this idea is critically evaluated in light of recent structural imaging data.The relative potency of drug and nondrug rewards is considered, alongside evidence that cognitive distortions in the processing of chance (for example, the illusion of control and the gambler's fallacy) may constitute an important added ingredient in gambling.

View Article: PubMed Central - PubMed

Affiliation: Department of Psychology, Centre for Gambling Research, University of British Columbia, Vancouver, Canada.

Show MeSH
Related in: MedlinePlus