Ventral striatal dopamine transporter availability is associated with lower trait motor impulsivity in healthy adults

Smith, Christopher T.; Juan, M. Danica San; Dang, Linh C.; Katz, Daniel T; Perkins, Scott F.; Burgess, Leah; Cowan, Ronald L.; Manning, H. Charles; Nickels, Michael L.; Claassen, Daniel O.; Samanez-Larkin, Gregory R.; Zald, David H.

doi:10.1038/s41398-018-0328-y

Cited by 17 publications

(11 citation statements)

References 92 publications

(135 reference statements)

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“…Young people with internet addiction had a lower DAT binding 33 and a reduced D2 receptor availability 34 in the ventral striatum. Interestingly, a reduced DAT density was also found in healthy individuals with higher trait impulsivity 35 . Furthermore, a reduced dopamine synthesis capacity was also found in cocaine addicts 36 , cannabis users 37 , and binge eaters 38 .…”

Section: Evidence For a Premorbid Vulnerability To Icdsmentioning

confidence: 85%

Unlucky punches: the vulnerability-stress model for the development of impulse control disorders in Parkinson’s disease

Theis

Probst

Fernagut

et al. 2021

npj Parkinsons Dis.

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Impulse-control disorders are commonly observed during dopamine-replacement therapy in Parkinson’s disease, but the majority of patients seems “immune” to this side effect. Epidemiological evidence suggests that a major risk factor may be a specific difference in the layout of the dopaminergic-reinforcement system, of which the ventral striatum is a central player. A series of imaging studies of the dopaminergic system point toward a presynaptic reduction of dopamine-reuptake transporter density and dopamine synthesis capacity. Here, we review current evidence for a vulnerability-stress model in which a relative reduction of dopaminergic projections to the ventral striatum and concomitant sensitization of postsynaptic neurons represent a predisposing (hypodopaminergic) vulnerability. Stress (hyperdopaminergic) is delivered when dopamine replacement therapy leads to a relative overdosing of the already-sensitized ventral striatum. These alterations are consistent with consecutive changes in reinforcement mechanisms, which stimulate learning from reward and impede learning from punishment, thereby fostering the development of impulse-control disorders. This vulnerability-stress model might also provide important insights into the development of addictions in the non-Parkinsonian population.

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Section: Evidence For a Premorbid Vulnerability To Icdsmentioning

confidence: 85%

Unlucky punches: the vulnerability-stress model for the development of impulse control disorders in Parkinson’s disease

Theis

Probst

Fernagut

et al. 2021

npj Parkinsons Dis.

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show abstract

“…This question is of particular interest because motor and choice impulsivity might at least in part be supported by common neural systems. First, DA in fronto-striatal circuits plays a role in both motor control [16,17] and choice impulsivity [18][19][20]. Second, some studies have suggested that lateral prefrontal cortical (LPFC) regions might support impulse control functions, both in motor and non-motor domains [21][22][23][24].…”

Section: Introductionmentioning

confidence: 99%

Temporal discounting in adolescents and adults with Tourette syndrome

et al. 2021

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Tourette syndrome is a neurodevelopmental disorder associated with hyperactivity in dopaminergic networks. Dopaminergic hyperactivity in the basal ganglia has previously been linked to increased sensitivity to positive reinforcement and increases in choice impulsivity. In this study, we examine whether this extends to changes in temporal discounting, where impulsivity is operationalized as an increased preference for smaller-but-sooner over larger-but-later rewards. We assessed intertemporal choice in two studies including nineteen adolescents (age: mean[sd] = 14.21[±2.37], 13 male subjects) and twenty-five adult patients (age: mean[sd] = 29.88 [±9.03]; 19 male subjects) with Tourette syndrome and healthy age- and education matched controls. Computational modeling using exponential and hyperbolic discounting models via hierarchical Bayesian parameter estimation revealed reduced temporal discounting in adolescent patients, and no evidence for differences in adult patients. Results are discussed with respect to neural models of temporal discounting, dopaminergic alterations in Tourette syndrome and the developmental trajectory of temporal discounting. Specifically, adolescents might show attenuated discounting due to improved inhibitory functions that also affect choice impulsivity and/or the developmental trajectory of executive control functions. Future studies would benefit from a longitudinal approach to further elucidate the developmental trajectory of these effects.

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“…Dopamine upregulation in the striatum is associated with impulsivity. Specifically, ventral striatal dopamine transporter availability is associated with lower trait motor impulsivity in healthy adults [ 50 ]. Impulsivity may then contribute to increased vulnerability to drug abuse [ 51 ].…”

Section: Discussionmentioning

confidence: 99%

Cannabinoid Receptor Type 1 Regulates Drug Reward Behavior via Glutamate Decarboxylase 67 Transcription

Seo

Park

et al. 2021

IJMS

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Interaction of cannabinoid receptor type 1 (CB1) and GABAergic neuronal activity is involved in drug abuse-related behavior. However, its role in drug-dependent Pavlovian conditioning is not well understood. In this study, we aimed to evaluate the effects of a CB1 agonist, JWH-210, on the development of conditioned place preference (CPP)-induced by methamphetamine (METH). Pretreatment with a synthetic cannabinoid, JWH-210 (CB1 agonist), increased METH-induced CPP score and METH-induced dopamine release in acute striatal slices. Interestingly, CB1 was expressed in glutamate decarboxylase 67 (GAD67) positive cells, and overexpression of CB1 increased GAD67 expression, while CB1 knockdown reduced GAD67 expression in vivo and in vitro. GAD67 is known as an enzyme involved in the synthesis of GABA. CB1 knockdown in the mice striatum increased METH-induced CPP. When GAD67 decreased in the mice striatum, mRNA level of CB1 did not change, suggesting that CB1 can regulate GAD67 expression. GAD67 knockdown in the mouse striatum augmented apomorphine (dopamine receptor D2 agonist)–induced climbing behavior and METH-induced CPP score. Moreover, in the human brain, mRNA level of GAD67 was found to be decreased in drug users. Therefore, we suggest that CB1 potentiates METH-induced CPP through inhibitory GABAergic regulation of dopaminergic neuronal activity.

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Ventral striatal dopamine transporter availability is associated with lower trait motor impulsivity in healthy adults

Cited by 17 publications

References 92 publications

Unlucky punches: the vulnerability-stress model for the development of impulse control disorders in Parkinson’s disease

Unlucky punches: the vulnerability-stress model for the development of impulse control disorders in Parkinson’s disease

Temporal discounting in adolescents and adults with Tourette syndrome

Cannabinoid Receptor Type 1 Regulates Drug Reward Behavior via Glutamate Decarboxylase 67 Transcription

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