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Introduction: We have previously shown that an interaction between medial prefrontal and parietal cortices is instrumental in promoting self-awareness via synchronizing oscillations in the gamma range. The synchronization of these oscillations is modulated by dopamine release. Given that such oscillations result from intermittent GABA stimulation of pyramidal cells, it is of interest to determine whether the dopaminergic system regulates GABA release directly in cortical paralimbic regions. Here, we test the hypothesis that the regulation of the GABA-ergic system by the dopaminergic system becomes attenuated in problem gamblers resulting in addictive behaviors and impaired self-awareness., Methods: [ 11 C]Ro15-4513 PET, a marker of benzodiazepine α1/α5 receptor availability in the GABA receptor complex, was used to detect changes in synaptic GABA levels after oral doses of 100mg L-dopa in a double-blind controlled study of male problem gamblers (N = 10) and age-matched healthy male controls (N = 10)., Results: The mean reduction of cortical gray matter GABA/BDZ receptor availability induced by L-dopa was significantly attenuated in the problem gambling group compared to the healthy control group (p = 0.0377)., Conclusions: Our findings demonstrate that: (a) Exogenous dopamine can induce synaptic GABA release in healthy controls. (b) This release is attenuated in frontal cortical areas of males suffering from problem gambling, possibly contributing to their loss of inhibitory control. This suggests that dysfunctional dopamine regulation of GABA release may contribute to problem gambling and gambling disorder., (© 2019 Aarhus University Hospital, Nuclear Medicine and PET. Brain and Behavior published by Wiley Periodicals, Inc.)

The incentive sensitization theory is a promising model for understanding the mechanisms underlying drug addiction, and has received support in animal and human studies. So far the theory has not been applied to the case of behavioral addictions like Gambling Disorder, despite sharing clinical symptoms and underlying neurobiology. We examine the relevance of this theory for Gambling Disorder and point to predictions for future studies. The theory promises a significant contribution to the understanding of behavioral addiction and opens new avenues for treatment., (Copyright © 2014 Elsevier Ltd. All rights reserved.)

The introduction of magnetoencephalography has made it possible to study electromagnetic signaling in deeper, paralimbic cortical structures such as the medial prefrontal/anterior cingulate (ACC) and medial parietal/posterior cingulate (PCC) cortices. Self-awareness and self-control have been attributed to these regions. To test the hypothesis that they are dysfunctional in pathological gambling with poor self-control, we studied gamblers with and without previous stimulant abuse and age- and sex-matched controls. We found that pathological gamblers were more impulsive than controls in a stop-signal task and attributed this to changes in the activity of the paralimbic network: Pathological gamblers had reduced synchronization at rest in the high gamma range (55-100 Hz) compared with controls and failed to show an increase in gamma synchronization during rest compared with the task, as observed in controls. Subgroup analysis revealed that pathological gamblers without a history of stimulant abuse had lower PCC power during the stop-signal task compared with controls and gamblers with previous stimulant abuse. Furthermore, gamblers with a history of stimulant abuse had up to four times higher power at the ACC site during rest and the task compared with controls. In conclusion, pathological gamblers had higher impulsivity and functional paralimbic abnormalities, which could not be explained by a history of stimulant abuse. In addition, previous stimulant abuse had a marked effect on the amplitude of oscillatory brain activity in the ACC and PCC, suggesting long-term deleterious effects of repeated dopaminergic drug exposure. These consequences should be investigated in more detail in longitudinal studies.

The objective of this study was to investigate the relationship between gambling severity and depressive symptoms in pathological gamblers addicted to slot machines, with the hypothesis that comorbid depressive symptoms are associated with exacerbated gambling symptoms and behavior. Twenty controls and 20 pathological gamblers with different levels of depressive symptoms were studied during slot machine gambling. We found exacerbated gambling behavior in gamblers with high compared to low levels of depressive symptoms in terms of self-reported gambling urge (P < 0.01) and excitement from gambling (P < 0.05), number of games played (P < 0.01), and duration of gambling (P < 0.05). A correlation between depressive and gambling symptoms was found (r = 0.602, P < 0.01), thereby questioning which symptoms contribute to the exacerbated gambling behavior. Regression analyses showed that the symptoms influenced gambling behavior albeit in different ways. Although gambling symptoms predicted the rate of games played (P < 0.001), depressive symptoms predicted gambling urge (P < 0.01) and duration of gambling (P < 0.05). We discuss whether gambling symptoms only co-occur with other disorders; the need to look beyond the classification of pathological gambling as an impulse control disorder; and the potential role of anhedonia in depressed gamblers.