Influence of cocaine administration patterns on dopamine receptor regulation

Puig, Stéphanie; Marie, Nicolas; Benturquia, Nadia; Noble, Florence

doi:10.1007/s00213-014-3488-3

Cited by 12 publications

(6 citation statements)

References 32 publications

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“…The findings indicate that deficient D 2 /D 3 receptor availability may contribute to steep temporal discounting among individuals with substance use disorders, attention-deficit hyperactivity disorder, or obesity (for a review, see Bickel et al, 2012 ), and carriers of the A1 allele of the ANKK1 Taq1A polymorphism ( Eisenberg et al, 2007 ). This reasoning is supported by reports that rats treated chronically with MA or cocaine display evidence of greater discounting of delayed rewards than saline-treated rats ( Richards et al, 1999 ; Paine et al, 2003 ; Roesch et al, 2007 ; Mendez et al, 2010 ), as both of both of these stimulants induce persistent reductions in striatal D 2 /D 3 receptor availability in rats ( McCabe et al, 1987 ; Puig et al, 2014 ) and monkeys ( Nader et al, 2006 ; Groman et al, 2012 ) following chronic exposure.…”

Section: Discussionmentioning

confidence: 71%

“…Like steep temporal discounting, low striatal D 2 /D 3 receptor availability is observed among individuals with substance use disorders (for a review, see Trifilieff and Martinez, 2014 ), and has been linked with an increased likelihood of relapse ( Martinez et al, 2011 ; Wang et al, 2012 ). Chronic exposure to methamphetamine (MA) or cocaine induces persistent reductions in striatal D 2 /D 3 receptor availability in rats ( McCabe et al, 1987 ; Puig et al, 2014 ) and monkeys ( Nader et al, 2006 ; Groman et al, 2012 ), and rats treated chronically with either of these drugs exhibit greater temporal discounting than controls ( Richards et al, 1999 ; Paine et al, 2003 ; Roesch et al, 2007 ; Mendez et al, 2010 ). Humans with attention-deficit hyperactivity disorder or obesity—two other disorders that are associated with low striatal D 2 /D 3 receptor availability (for a review, see Trifilieff and Martinez, 2014 )—also display greater temporal discounting than healthy controls (for a review, see Bickel et al, 2012 ).…”

Section: Introductionmentioning

confidence: 99%

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Low Dopamine D2/D3 Receptor Availability is Associated with Steep Discounting of Delayed Rewards in Methamphetamine Dependence

Ballard

Mandelkern

Monterosso

et al. 2015

International Journal of Neuropsychopharmacology

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Background:Individuals with substance use disorders typically exhibit a predilection toward instant gratification with apparent disregard for the future consequences of their actions. Indirect evidence suggests that low dopamine D2-type receptor availability in the striatum contributes to the propensity of these individuals to sacrifice long-term goals for short-term gain; however, this possibility has not been tested directly. We investigated whether striatal D2/D3 receptor availability is negatively correlated with the preference for smaller, more immediate rewards over larger, delayed alternatives among research participants who met DSM-IV criteria for methamphetamine (MA) dependence.Methods:Fifty-four adults (n = 27 each: MA-dependent, non-user controls) completed the Kirby Monetary Choice Questionnaire, and underwent positron emission tomography scanning with [18F]fallypride.Results:MA users displayed steeper temporal discounting (p = 0.030) and lower striatal D2/D3 receptor availability (p < 0.0005) than controls. Discount rate was negatively correlated with striatal D2/D3 receptor availability, with the relationship reaching statistical significance in the combined sample (r = -0.291, p = 0.016) and among MA users alone (r = -0.342, p = 0.041), but not among controls alone (r = -0.179, p = 0.185); the slopes did not differ significantly between MA users and controls (p = 0.5).Conclusions:These results provide the first direct evidence of a link between deficient D2/D3 receptor availability and steep temporal discounting. This finding fits with reports that low striatal D2/D3 receptor availability is associated with a higher risk of relapse among stimulant users, and may help to explain why some individuals choose to continue using drugs despite knowledge of their eventual negative consequences. Future research directions and therapeutic implications are discussed.

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Section: Discussionmentioning

confidence: 71%

Section: Introductionmentioning

confidence: 99%

Low Dopamine D2/D3 Receptor Availability is Associated with Steep Discounting of Delayed Rewards in Methamphetamine Dependence

Ballard

Mandelkern

Monterosso

et al. 2015

International Journal of Neuropsychopharmacology

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“…Repeated-cocaine treatments is a popular paradigm to explore the mechanisms of cocaine addiction. Consecutive intraperitoneal injections for 7 or 14 days are commonly used in previous studies, which had been demonstrated neuroadaptational changes associated with cocaine addition (Feng et al, 2014; Puig et al, 2014). In the present study, animals received intraperitoneal injections of cocaine (Qinghai Pharmacoceutical, China) at a dose of 20 mg/kg/d during 9:00 to 11:00 a.m. for 14 consecutive days.…”

Section: Methodsmentioning

confidence: 99%

Dynamic Expression Changes in the Transcriptome of the Prefrontal Cortex after Repeated Exposure to Cocaine in Mice

et al. 2017

Front. Pharmacol.

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Prefrontal cortex (PFC)-dependent functions, such as executive function, explicit learning, and memory, are negatively affected in cocaine abusers and experimental animal models of cocaine treatment. However, its molecular mechanisms are less understood. In the present study, we performed transcriptome profiling of the dynamic changes in the PFC after repeated cocaine administration in mice. We found 463, 14, and 535 differentially expressed genes (DEGs) at 2 h, 24 h, and 7 days, respectively, after the withdrawal of chronic cocaine treatment. Time-series correlation analysis identified 5 clusters of statistically significant expression patterns. The expression levels of DEGs in Clusters 1 and 5 exhibited a gradual or fluctuant decrease, Cluster 2 exhibited an initial increase followed by a decrease or return to the baseline level, and Clusters 3 and 4 exhibited a fluctuant increase in the expression of DEGs. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that genes related to oxidative phosphorylation, ribosomes, and neurodegenerative disorder were enriched in Cluster 1; genes related to the mitogen activated protein kinase (MAPK), transforming growth factor (TGF)-β, insulin signaling, and circadian pathways were enriched in Cluster 2; genes related to plasticity-related pathways were enriched in Clusters 3 and 4; and genes related to the proteasome were enriched in Cluster 5. Our results suggest that maladaptive neural plasticity associated with psychostimulant dependence may be an ongoing degenerative process with dynamic changes in the gene network at different stages of withdrawal. Furthermore, it could be helpful to develop new therapeutic approaches according to different periods of abstinence.

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“…First, all those genes are highly and predominantly expressed in the human brain. Most of their proteins are involved in plasma membrane rearrangement, consistent with some of the key mechanisms associated with non-motor aspects of tolerance to cocaine, including changes in receptor density 54 – 56 , dendritic growth, and synaptic plasticity (for reviews, see refs. 57 , 58 ).…”

Section: Discussionmentioning

confidence: 84%

Translational study of the whole transcriptome in rats and genetic polymorphisms in humans identifies LRP1B and VPS13A as key genes involved in tolerance to cocaine-induced motor disturbances

et al. 2020

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Motor disturbances strongly increase the burden of cocaine use disorder (CUDs). The objective of our translational study was to identify the genes and biological pathways underlying the tolerance to cocaine-induced motor effects. In a 5-day protocol measuring motor tolerance to cocaine in rats (N = 40), modeling the motor response to cocaine in patients, whole-genome RNA sequencing was conducted on the ventral and dorsal striatum to prioritize a genetic association study in 225 patients with severe CUD who underwent thorough phenotypic (cocaine-induced hyperlocomotion, CIH; and cocaine-induced stereotypies, CIS) and genotypic [571,000 polymorphisms (SNPs)] characterization. We provide a comprehensive description of the rat striatal transcriptomic response to cocaine in our paradigm. Repeated vs. acute cocaine binge administration elicited 27 differentially expressed genes in the ventral striatum and two in the dorsal striatum. One gene, Lrp1b, was differentially expressed in both regions. In patients, LRP1B was significantly associated with both CIS and CIH. CIH was also associated with VPS13A, a gene involved in a severe neurological disorder characterized by hyperkinetic movements. The LRP1B minor allele rs7568970 had a significant protective effect against CIS (558 SNPs, Bonferroni-corrected p = 0.02) that resisted adjustment for confounding factors, including the amount of cocaine use (adjusted beta = −0.965 and −2.35 for heterozygotes and homozygotes, respectively, p < 0.01). Using hypothesis-free prioritization of candidate genes along with thorough methodology in both the preclinical and human analysis pipelines, we provide reliable evidence that LRP1B and VPS13A are involved in the motor tolerance to cocaine in CUD patients, in line with their known pathophysiology.

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Influence of cocaine administration patterns on dopamine receptor regulation

Abstract: Two cocaine administration patterns induce different modifications of the dopaminergic receptor densities.

Cited by 12 publications

References 32 publications

Low Dopamine D2/D3 Receptor Availability is Associated with Steep Discounting of Delayed Rewards in Methamphetamine Dependence

Low Dopamine D2/D3 Receptor Availability is Associated with Steep Discounting of Delayed Rewards in Methamphetamine Dependence

Dynamic Expression Changes in the Transcriptome of the Prefrontal Cortex after Repeated Exposure to Cocaine in Mice

Translational study of the whole transcriptome in rats and genetic polymorphisms in humans identifies LRP1B and VPS13A as key genes involved in tolerance to cocaine-induced motor disturbances

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