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We asked if sensation-seeking is linked to premorbid personality characteristics in patients with addictive disorders, or the characteristics follow the sensation-seeking activity. We interpreted the former as a state associated with normal rates of dopamine synthesis, and the latter as a trait of individuals with abnormally high rates of synthesis. We previously determined dopaminergic receptor density in striatum, and we now tested the hypothesis that an elevated dopaminergic condition with increased extracellular dopamine and receptor density follows increased dopamine synthesis capacity in highly sensation-seeking individuals, as measured by positron emission tomography of 18 men with tracer fluorodopa (FDOPA). We detected a site in left caudate nucleus where the volume of distribution of FDOPA-derived metabolites correlated negatively with FDOPA metabolite turnover, consistent with decreased metabolite breakdown in highly sensation-seeking subjects. High rates of sensation-seeking attenuated the dopamine turnover in association with a low rate of dopamine recycling, low dopamine oxidation, and elevated extracellular dopamine and receptors in caudate nucleus. In contrast, low rates of sensation-seeking were associated with rapid dopamine recycling, rapid dopamine oxidation, low extracellular dopamine, and low receptor density. We conclude that the modulation of dopaminergic neurotransmission associated with sensation-seeking is a state of sensation-seeking, rather than a trait of personality following abnormal regulation of dopaminergic neurotransmission.

Pornography consumption is highly prevalent, particularly among young adult males. For some individuals, problematic pornography use (PPU) is a reason for seeking treatment. Despite the pervasiveness of pornography, PPU appears under-investigated, including with respect to the underlying neural mechanisms. Using functional magnetic resonance imaging (fMRI), we examined ventral striatal responses to erotic and monetary stimuli, disentangling cue-related 'wanting' from reward-related 'liking' among 28 heterosexual males seeking treatment for PPU and 24 heterosexual males without PPU. Subjects engaged in an incentive delay task in the scanner, in which they received erotic or monetary rewards preceded by predictive cues. Blood-oxygen-level-dependent responses to erotic and monetary cues were analyzed and examined with respect to self-reported data on sexual activity collected over the 2 preceding months. Men with and without PPU differed in their striatal responses to cues predicting erotic pictures but not in their responses to erotic pictures. PPU subjects when compared with control subjects showed increased activation of ventral striatum specifically for cues predicting erotic pictures but not for cues predicting monetary gains. Relative sensitivity to cues predicting erotic pictures vs monetary gains was significantly related to the increased behavioral motivation to view erotic images (suggestive of higher 'wanting'), severity of PPU, amount of pornography use per week, and number of weekly masturbations. Our findings suggest that, similar to what is observed in substance and gambling addictions, the neural and behavioral mechanisms associated with the anticipatory processing of cues specifically predicting erotic rewards relate importantly to clinically relevant features of PPU. These findings suggest that PPU may represent a behavioral addiction and that interventions helpful in targeting behavioral and substance addictions warrant consideration for adaptation and use in helping men with PPU.

•SVA symptoms were negatively correlated with LA.•Drift rate mediated the association between SVA symptoms and LA.•Brain activation patterns within cognitive control and motor networks shaped decision-making biases related to addiction. Excessive use of short-video platforms not only impairs decision-making processes but also predisposes individuals to addictive behaviors. This study investigated the relationship between short-video addiction (SVA) symptoms and loss aversion (LA), delving into the underlying computational and neural mechanisms using the drift diffusion model (DDM) and the inter-subject representational similarity analysis (IS-RSA). Behavioral analyses revealed a significant negative correlation between SVA symptoms and the LA coefficient (lnλ). Additionally, the DDM-based drift rate (v) was found to mediate this relationship. Neuroimaging analyses further indicated that SVA symptoms were negatively associated with gain-related activity in the right precuneus, while positively correlating with loss-related activity in the right cerebellum and left postcentral gyrus. Notably, precuneus activation during gain processing mediated the relationship between SVA symptoms and both lnλ and drift rate. IS-RSA revealed that inter-subject variations in SVA symptoms were significantly associated with distinct activation patterns related to gain processing in the frontoparietal network (e.g., frontal pole, inferior frontal gyrus, and supramarginal gyrus) and motor network (e.g., precentral), as well as loss-related activation patterns in the motor networks (e.g., postcentral and pre-supplementary motor area). Similar patterns emerged when examining simultaneous gain and loss-related activation patterns. Mediation analyses further demonstrated that functional activation patterns in the motor network mediated the relationships between inter-subject variations in SVA symptoms and both loss-aversion and psychological processing patterns (e.g., decision threshold, drift rate, and non-decision time). These findings provide novel insights into the cognitive and neural mechanisms underlying the influence of SVA symptoms on loss aversion, and suggest the critical roles of evidence accumulation speed and specific brain activation patterns—particularly within the cognitive control and motor network—in shaping decision-making biases associated with addiction.

Cannabis is the most commonly used substance of abuse in the United States after alcohol and tobacco. With a recent increase in the rates of cannabis use disorder (CUD) and a decrease in the perceived risk of cannabis use, it is imperative to assess the addictive potential of cannabis. Here we evaluate cannabis use through the neurobiological model of addiction proposed by Koob and Volkow. The model proposes that repeated substance abuse drives neurobiological changes in the brain that can be separated into three distinct stages, each of which perpetuates the cycle of addiction. Here we review previous research on the acute and long-term effects of cannabis use on the brain and behavior, and find that the three-stage framework of addiction applies to CUD in a manner similar to other drugs of abuse, albeit with some slight differences. These findings highlight the urgent need to conduct research that elucidates specific neurobiological changes associated with CUD in humans.

Behavioral addiction (BA) and substance use disorder (SUD) share similarities and differences in clinical symptoms, cognitive functions, and behavioral attributes. However, little is known about whether and how functional networks in the human brain manifest commonalities and differences between BA and SUD. Voxel-wise meta-analyses of resting-state functional connectivity (rs-FC) were conducted in BA and SUD separately, followed by quantitative conjunction analyses to identify the common and distinct alterations across both the BA and SUD groups. A total of 92 datasets with 2444 addicted patients and 2712 healthy controls (HCs) were eligible for the meta-analysis. Our findings demonstrated that BA and SUD exhibited common alterations in rs-FC between frontoparietal network (FPN) and other high-level neurocognitive networks (i.e. default mode network (DMN), affective network (AN), and salience network (SN)) as well as hyperconnectivity between SN seeds and the Rolandic operculum in SSN. In addition, compared with BA, SUD exhibited several distinct within- and between-network rs-FC alterations mainly involved in the DMN and FPN. Further, altered within- and between-network rs-FC showed significant association with clinical characteristics such as the severity of addiction in BA and duration of substance usage in SUD. The common rs-FC alterations in BA and SUD exhibited the relationship with consistent aberrant behaviors in both addiction groups, such as impaired inhibition control and salience attribution. By contrast, the distinct rs-FC alterations might suggest specific substance effects on the brain neural transmitter systems in SUD.

A growing body of preclinical and clinical literature suggests that brain-gut-microbiota interactions play an important role in human health and disease, including hedonic food intake and obesity. We performed a tripartite network analysis based on graph theory to test the hypothesis that microbiota-derived fecal metabolites are associated with connectivity of key regions of the brain's extended reward network and clinical measures related to obesity. DTI and resting state fMRI imaging was obtained from 63 healthy subjects with and without elevated body mass index (BMI) (29 males and 34 females). Subjects submitted fecal samples, completed questionnaires to assess anxiety and food addiction, and BMI was recorded. The study results demonstrate associations between fecal microbiota-derived indole metabolites (indole, indoleacetic acid, and skatole) with measures of functional and anatomical connectivity of the amygdala, nucleus accumbens, and anterior insula, in addition to BMI, food addiction scores (YFAS) and anxiety symptom scores (HAD Anxiety). The findings support the hypothesis that gut microbiota-derived indole metabolites may influence hedonic food intake and obesity by acting on the extended reward network, specifically the amygdala-nucleus accumbens circuit and the amygdala-anterior insula circuit. These cross sectional, data-driven results provide valuable information for future mechanistic studies.

More males than females play video games and develop problems with gaming. However, little is known regarding how males and females who game on the Internet may differ with respect to neural responses to gaming cues. Behavioral and functional magnetic resonance imaging (fMRI) data were recorded from 40 female and 68 male Internet gamers. This study included three components including participation in a pre-gaming cue-craving task, 30 min of online gaming and a post-gaming cue-elicited-craving task. Group differences were examined at pre-gaming, post-gaming and post- vs pre-gaming times. Correlations between brain responses and behavioral performance were calculated. : Gaming-related cues elicited higher cravings in male vs female subjects. Prior to gaming, males demonstrated greater activations in the striatum, orbitofrontal cortex (OFC), inferior frontal cortex and bilateral declive. Following gaming, male subjects demonstrated greater activations in the medial frontal gyrus and bilateral middle temporal gyri. In a post-pre comparison, male subjects demonstrated greater thalamic activation than did female subjects. Short-term gaming elicited in males vs females more craving-related activations to gaming cues. These results suggest neural mechanisms for why males may be more vulnerable than females in developing Internet gaming disorder.

Although behavioral addictions share many clinical features with drug addictions, they show strikingly large variation in their behavioral phenotypes (such as in uncontrollable gambling or eating). Neurotransmitter function in behavioral addictions is poorly understood, but has important implications in understanding its relationship with substance use disorders and underlying mechanisms of therapeutic efficacy. Here, we compare opioid and dopamine function between two behavioral addiction phenotypes: pathological gambling (PG) and binge eating disorder (BED). Thirty-nine participants (15 PG, 7 BED, and 17 controls) were scanned with [ C]carfentanil and [ F]fluorodopa positron emission tomography using a high-resolution scanner. Binding potentials relative to non-displaceable binding (BP ) for [ C]carfentanil and influx rate constant (K ) values for [ F]fluorodopa were analyzed with region-of-interest and whole-brain voxel-by-voxel analyses. BED subjects showed widespread reductions in [ C]carfentanil BP in multiple subcortical and cortical brain regions and in striatal [ F]fluorodopa K compared with controls. In PG patients, [ C]carfentanil BP was reduced in the anterior cingulate with no differences in [ F]fluorodopa K compared with controls. In the nucleus accumbens, a key region involved in reward processing, [ C]Carfentanil BP was 30-34% lower and [ F]fluorodopa K was 20% lower in BED compared with PG and controls (p<0.002). BED and PG are thus dissociable as a function of dopaminergic and opioidergic neurotransmission. Compared with PG, BED patients show widespread losses of mu-opioid receptor availability together with presynaptic dopaminergic defects. These findings highlight the heterogeneity underlying the subtypes of addiction and indicate differential mechanisms in the expression of pathological behaviors and responses to treatment.

Difficulties in emotion regulation are commonly reported among individuals with alcohol and drug addictions and contribute to the acquisition and maintenance of addictive behaviors. Alterations in neural processing of negative affective stimuli have further been demonstrated among individuals with addictions. However, it is unclear whether these alterations are a general feature of addictions or are a result of prolonged exposure to drugs of abuse. To test the hypothesis of altered negative affect processing independent of drug effects, this study assessed neural function among drug-naïve youth with a behavioral addiction--Internet gaming disorder (IGD). Fifty-six young adults (28 with IGD, 28 matched controls) participated in fMRI scanning during performance of a well-validated emotion regulation task. Between-group differences in neural activity during task performance were assessed using a whole-brain, mixed-effects ANOVA with correction for multiple comparisons at currently recommended thresholds (voxel-level p<0.001, pFWE<0.05). Compared to controls, youth with IGD exhibited significantly blunted neural responses within distributed subcortical and cortical regions including the striatum, insula, lateral prefrontal cortex and anterior cingulate in response to negative affective cues, as well as during emotion regulation. Independent component analysis (ICA) further identified between-group differences in engagement of a fronto-cingulo-parietal network, involving decreased engagement in IGD youth relative to controls. Study findings are largely consistent with those from prior neuroimaging studies in substance-use disorders, thus raising the possibility that neural processing of negative affect may be blunted across drug and behavioral addictions independent of acute or chronic drug effects.

Gambling disorder (GD) was reclassified as a behavioral addiction in the DSM-5 and shares clinical and behavioral features with substance use disorders (SUDs). Neuroimaging studies of GD hold promise in isolating core features of the addiction syndrome, avoiding confounding effects of drug neurotoxicity. At the same time, a neurobiologically-grounded theory of how behaviors like gambling can become addictive remains lacking, posing a significant hurdle for ongoing decisions in addiction nosology. This article integrates research on reward-related brain activity (functional MRI) and neurotransmitter function (PET) in GD, alongside the consideration of structural MRI data as to whether these signals more likely reflect pre-existing vulnerability or neuroadaptive change. Where possible, we point to qualitative similarities and differences with established markers for SUDs. Structural MRI studies indicate modest changes in regional gray matter volume and diffuse reductions in white matter integrity in GD, contrasting with clear structural deterioration in SUDs. Functional MRI studies consistently identify dysregulation in reward-related circuitry (primarily ventral striatum and medial prefrontal cortex), but evidence is mixed as to the direction of these effects. The need for further parsing of reward sub-processes is emphasized, including anticipation vs outcome, gains vs. losses, and disorder-relevant cues vs natural rewards. Neurotransmitter PET studies indicate amplified dopamine (DA) release in GD, in the context of minimal differences in baseline DA D2 receptor binding, highlighting a distinct profile from SUDs. Preliminary work has investigated further contributions of opioids, GABA and serotonin. Neuroimaging data increasingly highlight divergent profiles in GD vs. SUDs. The ability of gambling to perpetually activate DA (via maximal uncertainty) may contribute to neuroimaging similarities between GD and SUDs, whereas the supra-physiological DA effects of drugs may partly explain differences in the neuroimaging profile of the two syndromes. Coupled with consistent observations of correlations with gambling severity and related clinical variables within GD samples, the overall pattern of effects is interpreted as a likely combination of shared vulnerability markers across GD and SUDs, but with further experience-dependent neuroadaptive processes in GD.