ArticleNeuropharmacology2010
Cocaine exposure modulates dopamine and adenosine signaling in the fetal brain.
Article in Neuropharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
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
18 citing papers in PubMed, 39 citations in OpenAlex.
- Article
- Sleep Disorder and Cocaine Abuse Impact Purine and Pyrimidine Nucleotide Metabolic Signatures.Metabolites · 2022Article
- Modulation of lymphatic transport in the central nervous system.Theranostics · 2022Review
- Development of prefrontal cortex.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2022Review
- Allosteric Interactions between Adenosine AInternational journal of molecular sciences · 2021Review
- Molecular Integration in Adenosine Heteroreceptor Complexes Through Allosteric and De-Phosphorylation (STEP) Mechanisms and its Role in Brain Disease.Frontiers in pharmacology · 2021Article
- Single Cocaine Exposure Inhibits GABA Uptake via Dopamine D1-Like Receptors in Adolescent Mice Frontal Cortex.Neurotoxicity research · 2020Article
- Placental Barrier and Autism Spectrum Disorders: The Roles of Prolactin and Dopamine in the Developing Fetal Brain-Part II.Innovations in clinical neuroscience · 2019Article
- Dose response of acute cocaine on sleep/waking behavior in mice.Neurobiology of sleep and circadian rhythms · 2018Article
- The Role of Adenosine Receptors in Psychostimulant Addiction.Frontiers in pharmacology · 2017Review
- Cocaine-induced neurodevelopmental deficits and underlying mechanisms.Birth defects research. Part C, Embryo today : reviews · 2016Review
- Reversal Learning Deficits Associated with Increased Frontal Cortical Brain-Derived Neurotrophic Factor Tyrosine Kinase B Signaling in a Prenatal Cocaine Exposure Mouse Model.Developmental neuroscience · 2016Article
- Prenatal Cocaine Exposure Upregulates BDNF-TrkB Signaling.PloS one · 2016Article
- Cocaine-induced changes of synaptic transmission in the striatum are modulated by adenosine A2A receptors and involve the tyrosine phosphatase STEP.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2014Article
- Article
- Cocaine alters BDNF expression and neuronal migration in the embryonic mouse forebrain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Structural, metabolic, and functional brain abnormalities as a result of prenatal exposure to drugs of abuse: evidence from neuroimaging.Neuropsychology review · 2010Review
- A transgenic mouse model of neuroepithelial cell specific inducible overexpression of dopamine D1-receptor.Neuroscience · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Exposure to cocaine during the fetal period can produce significant lasting changes in the structure and function of the brain. Cocaine exerts its effects on the developing brain by blocking monoamine transporters and impairing monoamine receptor signaling. Dopamine is a major central target of cocaine. In a mouse model, we show that cocaine exposure from embryonic day 8 (E8) to E14 produces significant reduction in dopamine transporter activity, attenuation of dopamine D1-receptor function and upregulation of dopamine D2-receptor function. Cocaine's effects on the D1-receptor are at the level of protein expression as well as activity. The cocaine exposure also produces significant increases in basal cAMP levels in the striatum and cerebral cortex. The increase in the basal cAMP levels was independent of dopamine receptor activity. In contrast, blocking the adenosine A2a receptor downregulated the basal cAMP levels in the cocaine-exposed brain to physiological levels, suggesting the involvement of adenosine receptors in mediating cocaine's effects on the embryonic brain. In support of this suggestion, we found that the cocaine exposure downregulated adenosine transporter function. We also found that dopamine D2- and adenosine A2a-receptors antagonize each other's function in the embryonic brain in a manner consistent with their interactions in the mature brain. Thus, our data show that prenatal cocaine exposure produces direct effects on both the dopamine and adenosine systems. Furthermore, the dopamine D2 and adenosine A2a receptor interactions in the embryonic brain discovered in this study unveil a novel substrate for cocaine's effects on the developing brain.
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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.