ArticleThe Journal of pharmacology and experimental therapeutics2009
Lack of cocaine self-administration in mice expressing a cocaine-insensitive dopamine transporter.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
65 citing papers in PubMed, 91 citations in OpenAlex.
- Neuropharmacology of levamisole and its phase I metabolites: lack of evidence for levamisole-cocaine interactions.Psychopharmacology · 2026Article
- Dopamine DThe Journal of pharmacology and experimental therapeutics · 2024Article
- A sex-specific effect of MFrontiers in molecular neuroscience · 2024Article
- Glucagon-like peptide-1 receptors in nucleus accumbens, ventral hippocampus, and lateral septum reduce alcohol reinforcement in mice.Experimental and clinical psychopharmacology · 2023Article
- Cocaine induces locomotor sensitization through a dopamine-dependent VTA-mPFC-FrA cortico-cortical pathway in male mice.Nature communications · 2023Article
- A high-affinity cocaine binding site associated with the brain acid soluble protein 1.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Kappa Opioid Receptor Mediated Differential Regulation of Serotonin and Dopamine Transporters in Mood and Substance Use Disorder.Handbook of experimental pharmacology · 2022Review
- Jugular Vein Catheter Design and Cocaine Self-Administration Using Mice: A Comprehensive Method.Frontiers in behavioral neuroscience · 2022Article
- Disruption of the PDZ domain-binding motif of the dopamine transporter uniquely alters nanoscale distribution, dopamine homeostasis, and reward motivation.The Journal of biological chemistry · 2021Article
- Novelty-induced hyperactivity and suppressed cocaine induced locomotor activation in mice lacking threonine 53 phosphorylation of dopamine transporter.Behavioural brain research · 2021Article
- Identification of the Risk Genes Associated With Vulnerability to Addiction: Major Findings From Transgenic Animals.Frontiers in neuroscience · 2021Review
- Sex-Specific Role for Egr3 in Nucleus Accumbens D2-Medium Spiny Neurons Following Long-Term Abstinence From Cocaine Self-administration.Biological psychiatry · 2020Article
- In Situ Regulated Dopamine Transporter Trafficking: There's No Place Like Home.Neurochemical research · 2020Review
- Characterization of genetically complex Collaborative Cross mouse strains that model divergent locomotor activating and reinforcing properties of cocaine.Psychopharmacology · 2020Article
- Caenorhabditis elegans as an in vivo Model to Assess Amphetamine Tolerance.Brain, behavior and evolution · 2020Article
- Dopamine and addiction: what have we learned from 40 years of research.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Variability in the Drug Response of MFrontiers in pharmacology · 2019Article
- Intravenous cocaine self-administration in a panel of inbred mouse strains differing in acute locomotor sensitivity to cocaine.Psychopharmacology · 2018Article
- Effects of muscarinic MPsychopharmacology · 2018Article
- Pronounced Hyperactivity, Cognitive Dysfunctions, and BDNF Dysregulation in Dopamine Transporter Knock-out Rats.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
5 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cocaine addiction is a worldwide public health problem for which there are no established treatments. The dopamine transporter (DAT) is suspected as the primary target mediating cocaine's abuse-related effects based on numerous pharmacological studies. However, in a previous study, DAT knockout mice were reported to self-administer cocaine, generating much debate regarding the importance of the DAT in cocaine's abuse-related effects. Here, we show that mice expressing a "knockin" of a cocaine-insensitive but functional DAT did not self-administer cocaine intravenously despite normal food-maintained responding and normal intravenous self-administration of amphetamine and a direct dopamine agonist. Our results have three implications. First, they imply a crucial role for high-affinity DAT binding of cocaine in mediating its reinforcing effects, reconciling mouse genetic engineering approaches with data from classic pharmacological studies. Second, they demonstrate the usefulness of knockin strategies that modify specific amino acid sequences within a protein. Third, they show that it is possible to alter the DAT protein sequence in such a way as to selectively target its interaction with cocaine, while sparing other behaviors dependent on DAT function. Thus, molecular engineering technology could advance the development of highly specialized compounds such as a dopamine-sparing "cocaine antagonist."
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.